@article {pmid42127905,
year = {2026},
author = {Shen, J and Sun, Z and Song, H and Pu, Y and Wang, P and Hailili, G and Huang, Y and Mei, Z and Chen, H and Huang, L and Yuan, C and Wang, X and Zheng, Y},
title = {Healthful plant-based diet, gut enterotype, and cognition in a rural Chinese elderly cohort: A longitudinal multi-omics study.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102797},
doi = {10.1016/j.xcrm.2026.102797},
pmid = {42127905},
issn = {2666-3791},
abstract = {The gut microbiome may shape how diet influences cognitive aging, but population-based evidence remains limited. In 784 older adults living in rural China (70-98 years old) with fecal metagenomics and structured dietary assessment, a modified healthful plant-based diet index (mHPDI) is associated with distinct gut microbial structure and taxonomic shifts (15 species, 17 genera). Among participants with repeated cognitive measurements, higher mHPDI is associated with better global cognition, with stronger benefits in participants with non-Prevotella-dominant enterotypes (highest versus lowest tertile β = 0.34, 95% confidence interval [CI], 0.16 to 0.52) than in those with a Prevotella-dominant enterotype (0.04, -0.22 to 0.29; p interaction = 0.04). Enterotype-associated differences in microbial metabolic pathways, including preQ0 and L-isoleucine biosynthesis, parallel this heterogeneity. Moreover, 12 circulating microbiota-related metabolites (primarily amino acids and short-chain fatty acids) are linked to mHPDI. A composite score comprising these metabolites mediates 11.0% of the mHPDI-cognition association (p mediation = 0.02), with branched-chain amino acids as major contributors. These findings suggest that gut microbial context may shape diet-cognition associations.},
}

@article {pmid42128003,
year = {2026},
author = {Gutsfeld, S and Wray, C and Schweiger, N and Röhrig, A and Paschke, H and Fu, Q and Kasmanas, JC and Abdulkadir, N and Kader, S and Rocha, U and Ebert, A and Tal, T},
title = {N-Ethyl Perfluorooctane Sulfonamide (N-EtFOSA) Exposure Alters Microbiome Composition and Causes Microbiome-Dependent Behavior Effects in Larval Zebrafish.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.5c16330},
pmid = {42128003},
issn = {1520-5851},
abstract = {We hypothesized that host-associated microorganisms can alter host behavior by modifying perfluorooctane sulfonamides to produce perfluorooctanesulfonic acid (PFOS) or other potentially neuroactive metabolites. Zebrafish larvae (Danio rerio) were exposed to PFOS (0.28-5 μM), N-ethyl perfluorooctane sulfonamide (N-EtFOSA, 0.07-1.25 μM), or perfluorooctane sulfonamido ammonium iodide (PFOSAmS, 0.83-15 μM) from 5 to 6 days post fertilization (dpf). This resulted in altered dark-phase swimming behavior at 8 dpf. Exposure to PFOS, or N-EtFOSA, but not PFOSAmS caused a similar shift in community structure. We exposed microbiome-depleted (axenic, AX), conventionally colonized (CC), or axenic conventionalized on day 1 (AC1) zebrafish larvae to N-EtFOSA (0.22-0.7 μM) from 5 to 6 dpf. In comparison to CC and AC1 larvae, AX-larvae did not exhibit concentration-dependent hypoactivity at 8 dpf. Chemical analysis at 7 dpf revealed a significant increase in N-EtFOSA levels in AX-larvae and AX-water samples, relative to colonized cohorts. The main metabolite detected was perfluorooctane sulfonamide (FOSA), which was not microbiome-dependent. Perfluorooctane sulfonamidoacetic acid (FOSAA) was detected at lower levels in AX-larvae, relative to colonized groups. This study revealed that the presence of the microbiome enhanced N-EtFOSA-dependent behavior effects at the level of the host. This supports the concept that chemical-microbiome interactions can influence host phenotypic outcomes.},
}

@article {pmid42128073,
year = {2026},
author = {Wang, X and Xi, J and Gong, H and Yin, Y and Jin, C and Zhao, Y and Wang, S and Zhao, D and Liu, S and Wang, W and Liu, M},
title = {Intestinal CncC gene activation mediates the sleep-protective effects of Ziziphus jujuba alcohol extract via the gut-brain axis in Drosophila.},
journal = {Journal of ethnopharmacology},
volume = {368},
number = {},
pages = {121859},
doi = {10.1016/j.jep.2026.121859},
pmid = {42128073},
issn = {1872-7573},
abstract = {Ziziphus jujuba var. spinosa (Bunge) Hu ex H.F.Chow (Ziziphus jujuba) has been used in Chinese folk medicine for over 2000 years, with the Shennong Bencao Jing noting that the "main worry is not sleeping." More than 100 health foods and Chinese patent medicines, feature Ziziphus jujuba as the core ingredient, embodying the traditional concept of "nourishing heart and tranquilizing mind."

OBJECTIVE: This study investigated microbiome-targeted phytotherapeutic strategies for sleep disorders, which are often linked to gut dysbiosis and systemic oxidative stress.

MATERIALS AND METHODS: Chronic sleep-deprived Drosophila were orally treated with a Ziziphus jujuba alcohol extract (ZJAE). Sleep architecture was recorded using a Drosophila activity monitor. Intestinal microbiota shifts were assessed by gnotobiotic colonization and 16S rRNA sequencing. Quantitative PCR, western blotting, and reactive oxygen species (ROS) imaging assessed intestinal signaling of the Nrf2 homolog cap 'n' collar C (CncC) gene, antioxidant gene expression, gut barrier integrity, and systemic ROS. Gut-specific RNA interference was used to targeted the CncC gene.

RESULTS: ZJAE restored total sleep time and reduced motor hyperactivity, consistent with reduced systemic ROS and restoration of intestinal barrier function. Acetobacter was enriched. Antibiotic-treated flies colonized with acetic acid bacteria and treated with ZJAE showed the highest CncC gene expression. Knockdown of the CncC gene knockdown in intestinal epithelial cells abolished improvements in both sleep parameters and redox status.

CONCLUSION: ZJAE recruits commensal Acetobacter to activate an intestinal Nrf2-dependent redox axis, normalizing oxidative stress-linked sleep deficits. These findings provide the first preclinical evidence of a microbiota-dependent mechanism, supporting a rationale for the development of jujube-based functional foods targeting oxidative sleep disorders.},
}

@article {pmid42128097,
year = {2026},
author = {Wang, R and Liang, C and Li, Y and Zhu, L},
title = {Insights into Lower Reproductive Tract Aging: Mechanisms and Perspectives.},
journal = {Mechanisms of ageing and development},
volume = {},
number = {},
pages = {112192},
doi = {10.1016/j.mad.2026.112192},
pmid = {42128097},
issn = {1872-6216},
abstract = {Rising global life expectancy intensifies the health impact of female lower reproductive tract aging, particularly affecting the uterus, cervix, and vagina. This process is primarily driven by estrogen depletion triggering hormonal imbalance, chronic inflammation, cellular senescence through senescence-associated secretory phenotype mediators, and systemic oxidative stress. These interconnected mechanisms accelerate structural degeneration leading to uterine fibrosis with endometrial atrophy, pelvic organ prolapse, cervical susceptibility to persistent HPV infections and subsequent malignancy development, vaginal microbiome disruption, and genitourinary syndrome of menopause. Future advances will require addressing the pronounced research imbalance across anatomical sites, resolving the causal links between immune aging and tissue-specific pathologies, and integrating multi-omics and organoid technologies to enable personalized, site-specific interventions.},
}

@article {pmid42128146,
year = {2026},
author = {Su, YJ and Kuo, BY and Lin, LY and Lin, YH and Chen, CC and Sheu, JJ},
title = {High fat diet-induced diversity reduction in gut microbiota facilitates the development of systemic lupus erythematosus.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {110398},
doi = {10.1016/j.jnutbio.2026.110398},
pmid = {42128146},
issn = {1873-4847},
abstract = {Systemic lupus erythematosus (SLE) is influenced by environmental, genetic, and dietary factors. The impact of a high-fat diet (HFD) on SLE pathogenesis remains unclear. To investigate this, we utilized an imiquimod (IMQ)-induced SLE mouse model under HFD and normal diet conditions. Mice receiving both HFD and IMQ exhibited aggravated inflammation, tissue damage, and enhanced B-cell infiltration in the colon, alongside significant reductions in gut microbial diversity. Notably, HFD alone induced similar microbiome and immune alterations, suggesting a pro-SLE intestinal microenvironment. Microbiome analysis identified specific species shifts, including Parabacteroides goldsteinii and Bacteroides caccae, associated with disease progression. Metabolomic profiling revealed dysregulation of several pathways, including amoebiasis, with marked reduction of dl-o-phosphoserine. These findings suggest that HFD-induced microbial and metabolic changes may exacerbate SLE development. Our study highlights the interplay between diet, gut microbiota, and immune regulation in SLE, providing potential targets for microbiome- or diet-based interventions.},
}

@article {pmid42128216,
year = {2026},
author = {Ackermann, RE and Brayton, KA and Oosthuizen, MC and Matthee, CA and Makgabo, SM and Ngoveni, H and Fagir, DM and van Wyk, I and Quan, V and Rossouw, J and Weyer, J and Blumberg, LH and Frean, J and Collins, NE},
title = {Microbial networks and pathogen detection: Insights from ticks and patients with acute febrile illness.},
journal = {Acta tropica},
volume = {},
number = {},
pages = {108138},
doi = {10.1016/j.actatropica.2026.108138},
pmid = {42128216},
issn = {1873-6254},
abstract = {Ticks are vectors of diverse pathogens, with transmission risk elevated in regions of close human-livestock-wildlife contact. In rural South Africa, non-malarial acute febrile illness (AFI) is common, yet the microbial diversity of ticks and human patients remains underexplored. We applied microbiome sequencing (16S rDNA for bacteria; 18S rDNA for eukaryotes) to four sample groups from Bushbuckridge, Mpumalanga, South Africa: Rhipicephalus sanguineus s.l. (n16S = 175, n18S = 30), Amblyomma hebraeum (n16S = 74, n18S = 21), human AFI patients (n16S = 168, n18S = 14), and apparently healthy humans (n16S = 67, n18S = 3). Bacterial alpha diversity did not differ significantly between groups (Shannon p = 0.81, Inverse-Simpson p = 0.36), whereas eukaryotic diversity was lower in human patients (Shannon p = 0.00026, Inverse-Simpson p = 0.00415). Beta diversity exhibited clear differences between groups, with ticks showing greater variability (bacteria p = 0.001; eukaryotes p = 0.001). Co-occurrence networks revealed structured clusters reflecting organised community interactions. Pathogen DNA detected included Plasmodium falciparum in an AFI patient, and sequences similar to several spotted fever group Rickettsia species, including the first report of Rickettsia barbariae in ticks from South Africa. This result requires confirmation by multi-gene sequence analysis. Novel Rickettsiales with uncertain pathogenicity were detected across sample groups. Opportunistic pathogens were detected including Acanthamoeba, Aspergillus and Malassezia. These findings provide baseline evidence on microbial diversity in a rural community in South Africa, underscoring the need for integrated surveillance to address AFI burden within a One Health framework.},
}

@article {pmid42128223,
year = {2026},
author = {Li, J and Jong, MC and Li, P and Yu, K and Bao, Y and Song, Z and Shen, Y and Yew-Hoong Gin, K and He, Y},
title = {Size-Dependent Toxicity Cascades of Microplastics in Perna viridis: Mechanistic Insights into Membrane Damage, Microbial Dysbiosis, and Persistent Genotoxicity.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {128330},
doi = {10.1016/j.envpol.2026.128330},
pmid = {42128223},
issn = {1873-6424},
abstract = {Microplastics are pervasive contaminants in coastal ecosystems, but their size-dependent toxicity cascades across multiple biological levels remain poorly resolved. This study integratively assesses the 0.5-, 5-, and 50-μm microplastics toxicity in Perna viridis through multi-endpoints (cellular membrane stability, microbial homeostasis, haemolymph DNA integrity) across exposure (14-day) and depuration (7-day), revealing a size-dependent cascade. Exposure to 0.5-μm MPs triggered intracellular organelle stress, leading to oxidative stress responses marked by elevated ROS and MDA along with progressive ATP depletion. This was accompanied by downregulation of cytoskeletal genes (Actin and Tubb4b) and upregulation of the membrane repair gene preCOL-p. Concurrently, 0.5-μm MPs triggered severe intestinal dysbiosis reflected in reduced Shannon and Chao indices, enrichment of virulence genes and significant haemolymph DNA damage as measured by the Genetic Damage Index. Although membrane biomarkers recovered after depuration, irreversible DNA damage persisted exclusively in the 0.5-μm groups. GO enrichment analysis showed consistent top functions across MPs sizes but divergence in lower-ranked terms, while KEGG analysis revealed distinct size-dependent upregulation of metabolic pathways in exposed microbial communities. We propose a size-dependent cascading toxicity framework in which internalized small MPs first perturb cell membranes, then drive microbiome dysbiosis and microbiome-derived inflammatory signals, ultimately leading to sustained DNA damage.},
}

@article {pmid42128400,
year = {2026},
author = {Han, E and Nam, JH and Lee, I and Ku, CR and Lee, YH},
title = {Metformin beyond Glycemic Control: New Mechanistic Insights and Expanding Therapeutic Horizons.},
journal = {Diabetes & metabolism journal},
volume = {50},
number = {3},
pages = {435-449},
pmid = {42128400},
issn = {2233-6087},
support = {2021F-4//Korean Diabetes Association/ ; RS-2024-00352467//National Research Foundation of Korea/ ; RS-2025-02214844//National Research Foundation of Korea/ ; //Ministry of Science and ICT/ ; },
mesh = {Humans ; *Metformin/therapeutic use/pharmacology ; *Hypoglycemic Agents/therapeutic use/pharmacology ; Gastrointestinal Microbiome/drug effects ; *Glycemic Control ; Aging/drug effects ; Animals ; Neoplasms/drug therapy ; },
abstract = {Metformin, while central to diabetes management, functions as a highly pleiotropic agent with mechanisms that extend far beyond simple glycemic control. In age-related degenerative diseases, including neurodegenerative disorders, it may modulate mitochondrial function, reduce oxidative stress, and influence longevity-related pathways, suggesting possible anti-aging effects. Emerging evidence also points to anticancer activity, with studies reporting reduced incidence and improved outcomes across several malignancies, potentially through mammalian target of rapamycin (mTOR) inhibition, metabolic reprogramming, and suppression of inflammatory signaling. Furthermore, the 'intestinal glucotonic effect' has been proposed to involve glucose excretion from the circulation into the gut lumen through reactive oxygen species-dependent upregulation and membrane localization of glucose transporter type 1 (GLUT1), an adenosine monophosphate-activated protein kinase (AMPK)-independent process that may contribute to the reprogramming of systemic glucose flux and provides metabolic substrates for the microbiota. Metformin also alters the gut microbiome by increasing the abundance of multiple short-chain fatty acid-producing bacteria and enhancing intestinal barrier function, which may contribute to systemic metabolic and immunologic benefits. Collectively, metformin is a pleiotropic agent with broad effects on aging biology, cancer pathophysiology, host-microbiome interactions, and immunometabolic regulation. Despite decades of clinical use, important gaps remain in understanding how these mechanisms converge to influence outcomes in individuals with diabetes and beyond.},
}

Humans
*Metformin/therapeutic use/pharmacology
*Hypoglycemic Agents/therapeutic use/pharmacology
Gastrointestinal Microbiome/drug effects
*Glycemic Control
Aging/drug effects
Animals
Neoplasms/drug therapy

@article {pmid42128407,
year = {2026},
author = {Pati, NB and Chung, BK and Holm, K and Sætre, F and Reims, HM and Aasebo, AT and Gedde-Dahl, T and Sreelakshmi, KV and Domanska, D and Hov, JR and Bækkevold, ES and Jahnsen, FL},
title = {Ultra long-lived plasma cells in the human small intestine produce microbiota-reactive IgA antibodies.},
journal = {Beneficial microbes},
volume = {},
number = {},
pages = {1-13},
doi = {10.1163/18762891-bja00120},
pmid = {42128407},
issn = {1876-2891},
abstract = {A large fraction of the intestinal microbiota is highly coated with secretory IgA, and bacteria-specific IgA is believed to shape the composition of the microbiota. A hallmark of the adaptive immune system is immunological memory to specific antigens. However, whether there is strong and persistent memory of secretory antibodies to bacterial antigens has not been determined. Here we show that ultra long-lived CD19-CD45- (age > 20 years) plasma cells (PCs) residing in the human small intestine produce IgA that binds to most taxa of a diverse anaerobic microbiota culture. Long-lived CD19-CD45+ (age > 10 years) and short-lived CD19+CD45+ (age < 2 years) PCs also produced IgA with broad bacterial reactivity. A clear correlation between high-binding and low-binding taxa was observed across the PC subsets. We also found that host PCs were depleted in acute intestinal graft versus host disease, a condition strongly associated with loss of microbiota diversity. Together, we show that bacterial antigens in the intestine induce an extremely stable, long-lasting humoral immune memory that may be important for the long-term stability and resilience of the intestinal microbiome.},
}

@article {pmid42128724,
year = {2026},
author = {Alam, A and Mayengbam, SS and Senchanthisai, S and Bektas, EI and Dey, P},
title = {Microbiome: a driver of pancreatic inflammation and tumorigenesis.},
journal = {Trends in cancer},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.trecan.2026.04.006},
pmid = {42128724},
issn = {2405-8025},
abstract = {The human microbiome plays a crucial role in regulating various physiological processes, including immune responses, inflammation, gut permeability, and overall homeostasis. Recent studies have identified bacterial and fungal components in the tumor microenvironment of multiple malignancies, including pancreatic ductal adenocarcinoma (PDAC). These intratumoral microbiomes drive tumorigenesis by activating oncogenic signaling cascades and reprogramming both innate and adaptive immune responses, ultimately establishing a protumorigenic niche. In this review, we highlight the advances, limitations, and challenges of studying the intratumoral microbiome and its cellular products in PDAC tumorigenesis, with a specific focus on their modulation of the immune axis. Finally, we evaluate existing and emerging therapeutic strategies, including microbiome-targeted drugs, antibiotics, probiotics, and engineered microbes, to disrupt protumorigenic microbial influences and improve clinical outcomes.},
}

@article {pmid42128741,
year = {2026},
author = {Lefranc, M and Ramel, E and Marsh, R and Tricker, JM and van der Gast, C and Bomberger, JM and Delhaes, L},
title = {Towards a gut-lung axis role in pwCF on CFTR modulators: rationale, clinical evidence and perspectives.},
journal = {Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jcf.2026.04.011},
pmid = {42128741},
issn = {1873-5010},
abstract = {Recent data support the existence of a "gut-lung axis" (GLA), yet it's role in chronic respiratory diseases, like cystic fibrosis (CF), is under investigation. In this review we explore the potential linkages and underlying mechanisms for gut-lung interaction axis, in terms of rationale (same embryonic and anatomical origins), microbial and immune interactions, and recent advances on GLA role in chronic lung diseases, with a focus on GLA research relevant to CF. The introduction of CFTR modulators has revolutionized CF management, dramatically reshaping the disease's clinical course by improving ion transport, mucosal hydration and mucociliary clearance. CFTR modulators are known to improve anion channel function, which has resulted in physiological and microbiological changes to the respiratory tract and gastrointestinal tract, which are likely to impact the GLA and are explored in this review. While there is a growing literature for the role of the GLA in regulating lung physiology in health and disease, additional work is warranted to elucidate molecular mechanisms by which the GLA mediates pathogenesis of disease. The ultimate goal would be to apply mechanistic understanding from the bench to the bedside to enable more personalized treatment strategies that both guide and improve lung disease management, especially in the CF field.},
}

@article {pmid42129074,
year = {2026},
author = {Veenstra, TD},
title = {The Pathology of Viral Infections.},
journal = {Advances in experimental medicine and biology},
volume = {1511},
number = {},
pages = {127-158},
pmid = {42129074},
issn = {0065-2598},
mesh = {Humans ; *Virus Diseases/pathology/virology ; Viruses/pathogenicity ; Microbiota ; Animals ; Host-Pathogen Interactions/physiology ; },
abstract = {If you were to ask, "Biologically speaking, what are humans made of?", almost everyone would reply "Human cells and molecules, of course." This seemingly logical answer, however, does not truly capture the diversity of the human organism. Over the past couple of decades scientists have discovered that humans are a collective of cohabitating human, bacteria, and fungi cells along with countless numbers of viruses. Collectively, these microorganisms are referred to as the microbiome (Lederberg and McCray, The Scientist 15:8, 2001). The most recent estimates suggest the biological material from these microorganisms makes up as much as half of every human. Considering the size of the microbiome, it is not surprising that humans share an intimate relationship with viruses since they will be found wherever life exists.},
}

Humans
*Virus Diseases/pathology/virology
Viruses/pathogenicity
Microbiota
Animals
Host-Pathogen Interactions/physiology

@article {pmid42129076,
year = {2026},
author = {Veenstra, TD},
title = {Proteomic Characterization of HIV Infection.},
journal = {Advances in experimental medicine and biology},
volume = {1511},
number = {},
pages = {189-222},
pmid = {42129076},
issn = {0065-2598},
mesh = {Humans ; *HIV Infections/metabolism/virology ; Male ; *Proteomics/methods ; Homosexuality, Male ; *HIV-1/metabolism ; },
abstract = {In the summer of 1981, young gay men began falling ill and dying of opportunistic infections. The strange thing was that these infections should have been easily rebuffed by their immune systems (Greene WC, Eur J Immunol 37(Suppl 1):S94-S102, 2007). These men become emaciated and developed dark purple lesions primarily on their arms and faces. These lesions were due to Kaposi's sarcoma, a relatively rare and aggressive form of cancer (Antman K and Chang Y, N Engl J Med 342:1027-1038, 2000). Physicians in cities such as New York, Los Angeles, and San Francisco were dumbfounded by the presence of young men who appeared elderly (Greene WC, Eur J Immunol 37(Suppl 1):S94-S102, 2007; Premeaux TA and Ndhlovu LC, Curr Opin HIV AIDS 18:237-245, 2023). Fear initially spread throughout the gay male community as this group was disproportionately impacted. As their health rapidly deteriorated, doctors were unable to prevent patients from dying from opportunistic infections and malignancies. The condition was recognized in 1981 as acquired immune deficiency syndrome (AIDS) (CDC, MMWR Morb Mortal Wkly Rep 30:305-308, 1981). As it became more publicized, the shock and stigma surrounding individuals who died from AIDS grew. The first major figure to reveal their AIDS diagnosis was Rock Hudson. This revelation was followed by other well-known individuals including Robert Reed (i.e., the father on the Brady Bunch), Arthur Ashe, and Freddie Mercury (webmd.com/hiv-aids/ss/slideshow-celebrities-hiv-aids).},
}

Humans
*HIV Infections/metabolism/virology
Male
*Proteomics/methods
Homosexuality, Male
*HIV-1/metabolism

@article {pmid42129181,
year = {2026},
author = {Dobranowski, P and Duan, H and Butcher, J and Mayne, J and Figeys, D and Mack, DR and Stintzi, A},
title = {Individual variability shapes ex vivo responses to resistant starch in inflammatory bowel disease derived microbiomes.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01003-w},
pmid = {42129181},
issn = {2055-5008},
support = {OGI-149//Government of Canada through Genome Canada and the Ontario Genomics Institute/ ; project number 13440//Ontario Ministry of Economic Development and Innovation/ ; },
abstract = {Fiber-based therapies focus on butyrate production, a process often dysregulated in inflammatory bowel disease (IBD), but seldomly examine other metabolites or functional pathways. Here, we systematically profiled ex vivo responses of 66 pediatric IBD microbiomes to nine resistant starches (RS), with extensive multi-omic characterization in a subset. Our study demonstrates that inter-individual variability dominates over RS-specific effects, yielding consistent yet highly personalized fermentation phenotypes, microbial compositional shifts, and metabolite outputs. Beyond butyrate, we identify previously unreported RS fermentation metabolites, revealing hidden functional pathways and cross-feeding interactions not captured by conventional short chain fatty acid-focused analyses. Metaproteomic profiling further revealed a coordinated shift from host mucin-degrading activity toward RS utilization. Together, these findings show that RS fermentation is shaped by both RS type and participant microbiome composition, and establish the RapidAIM ex vivo platform as a fiber personalization pipeline fit for interventions aimed at restoring microbial functions disrupted in human diseases.},
}

@article {pmid42129189,
year = {2026},
author = {Lacruz-Pleguezuelos, B and Pérez-Cuervo, A and Coleto-Checa, D and Bazán, GX and Romero-Tapiador, S and Freixer, G and Fernández-Cabezas, J and Aguilar-Aguilar, E and Martín-Segura, A and Cárdenas-Roig, N and Carrasco-Guijarro, L and Fernández, LP and Espinosa-Salinas, I and Ramírez de Molina, A and Morales, A and Tolosana, R and Ortega-Garcia, J and Pancaldi, V and Marcos-Zambrano, LJ and Carrillo de Santa Pau, E},
title = {Network topology of the gut microbiome associates with metabolic health in obesity.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42129189},
issn = {2041-1723},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics/physiology ; Male ; Female ; *Obesity/microbiology/metabolism ; Middle Aged ; Cross-Sectional Studies ; Adult ; Feces/microbiology ; Metagenomics ; *Obesity, Metabolically Benign/microbiology/metabolism ; Dysbiosis/microbiology ; Phenotype ; },
abstract = {Obesity is a heterogeneous condition comprising a continuum of phenotypes with various metabolic and inflammatory profiles. Metabolically healthy obesity (MHO) identifies individuals with obesity but a relatively preserved metabolic state, although little is known about the gut microbiome features underlying this phenotype. Here, we analyzed gut microbial network structures of 931 individuals living with metabolically healthy non-obesity (MHNO), MHO, metabolically unhealthy non-obesity (MUNO), and metabolically unhealthy obesity (MUO), performing cross-sectional analyses on feces shotgun metagenomics data. Individuals with MHNO and MHO harbor more robust and functionally cohesive microbial networks, while communities from MUO and MUNO phenotypes exhibit a potentially dysbiotic state with reduced connectivity. A nutritional intervention cohort showed an improvement in network connectivity in parallel with metabolic improvements. Our findings show differences in microbial connectivity and association patterns across metabolic and obesity phenotypes, shedding light on how distinct microbial network structures may associate with host metabolic health and disease.},
}

Humans
*Gastrointestinal Microbiome/genetics/physiology
Male
Female
*Obesity/microbiology/metabolism
Middle Aged
Cross-Sectional Studies
Adult
Feces/microbiology
Metagenomics
*Obesity, Metabolically Benign/microbiology/metabolism
Dysbiosis/microbiology
Phenotype

@article {pmid42129350,
year = {2026},
author = {Parkin, K and Christophersen, CT and Verhasselt, V and Palmer, DJ and Cooper, MN and Prescott, SL and Silva, D and Martino, D},
title = {Chlorinated drinking water exposure enriches antimicrobial resistance pathways in the infant gut microbiome: a randomized trial.},
journal = {Communications medicine},
volume = {},
number = {},
pages = {},
doi = {10.1038/s43856-026-01626-2},
pmid = {42129350},
issn = {2730-664X},
abstract = {BACKGROUND: Water chlorination is essential for controlling harmful microbes in drinking water; however, the antimicrobial effects of chlorine-based disinfectants present in tap water may influence early-life gut microbial ecology.

OBJECTIVE: To investigate the functional and compositional impact of chlorinated drinking water on the gut microbiome of infants.

DESIGN: The waTer qUality and Microbiome Study (TUMS) was an Australian-based double-blinded, randomised controlled trial. Six-month-old infants (n = 197) received either de-chlorinated drinking water via benchtop filtration (treatment, n = 99), or regular chlorinated water (control, n = 98) for twelve months. Tap water and stool samples were collected at baseline and at end of intervention. Metagenomic sequencing was used for faecal microbiome analysis. Primary outcomes were differences in gut microbiota between groups, secondary outcomes included incidence of allergic sensitization and respiratory conditions.

RESULTS: At baseline, 170 stool samples (83 control, 87 intervention) were collected, with 130 samples obtained at the end of the intervention (65 control, 65 intervention). Overall community structure was similar between groups after the intervention, including beta diversity (0.56% variance explained; p = 0.84), richness (-4.25, 95% CI; -14.85 to 6.35, p = 0.43) or Shannon Index (-0.14, 95% CI; -0.32 to 0.04, p = 0.12). The chlorinated water group showed enrichment of antibiotic resistance MetaCyc groups and pathways (adjusted p < 0.05). Stratified analysis suggested this effect was potentiated by clinical antibiotic use.

CONCLUSION: Chlorinated drinking water may enhance resistance functions in the infant gut microbiome. While remaining vital for public health, future studies should explore whether adjusting the timing or method of drinking water disinfectants into the infant diet can reduce selective pressures.

TRIAL REGISTRATION: ACTRN12619000458134; https://www.anzctr.org.au.},
}

@article {pmid42129442,
year = {2026},
author = {Shinde, RM and Kotasthane, AS and Agrawal, T},
title = {Bio decomposition of paddy straw waste using laccase producing novel soil bacterial isolates: An eco-friendly and sustainable approach.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-50628-6},
pmid = {42129442},
issn = {2045-2322},
abstract = {The soil microbiome plays a pivotal role in carbon sequestration, particularly through the degradation of lignocellulosic biomass such as paddy straw, which is often disposed of through environmentally harmful practices like open-field burning. This study investigates the isolation and characterization of novel lignocellulolytic bacterial strains capable of efficiently degrading paddy straw, thereby contributing to sustainable carbon management. A diverse collection of 27 bacterial isolates was obtained from soil samples, demonstrating significant cellulase, laccase, and lignin-degrading activities. Detailed biochemical and phenotypic analyses revealed distinct metabolic profiles and carbon source utilization patterns among the isolates. Notably, strains SH2A, AK17, AK15, U6, and SH2 achieved up to 94% degradation of paddy straw within 25 days, with isolate GS5A exhibiting an 18% reduction in recalcitrant lignin content in paddy straw within just 10 days leading to enhanced bioavailability of structural polysaccharides, and accelerating microbial-mediated degradation processes. Enzyme kinetic studies indicated optimal laccase activity at temperatures of 45-55 °C and pH levels of 4-7, with isolates TR32, SH2A, and AK17 producing laccase activities exceeding 90 U/L. Molecular characterization via 16 S rRNA sequencing identified these isolates as belonging to genera such as Pseudomonas, Enterobacter, Acinetobacter, and Klebsiella, known for their lignocellulolytic enzyme production. The findings underscore the potential of these bacterial strains exhibiting rapid lignin degradation enabling faster and more effective paddy straw decomposition compared to previously reported strains. Thereby leading faster carbon sequestration through effective biomass management, contributing to the development of a circular bio-economy and sustainable agricultural practices.},
}

@article {pmid42129646,
year = {2026},
author = {Mannan, SJ and Roqunuzzaman, M and Mannan, ABA and Begum, K and Yasmin, M and Yihune, E and Al-Mutairi, AA and Zaki, MEA and Ahsan, CR},
title = {Exploring genetic variations and plasmid diversity in Escherichia coli strains isolated from Hospital Wastewater.},
journal = {BMC genomics},
volume = {27},
number = {1},
pages = {},
pmid = {42129646},
issn = {1471-2164},
mesh = {*Wastewater/microbiology ; *Escherichia coli/genetics/isolation & purification/pathogenicity/classification ; *Plasmids/genetics ; *Genetic Variation ; Hospitals ; Polymorphism, Single Nucleotide ; Phylogeny ; Drug Resistance, Multiple, Bacterial/genetics ; beta-Lactamases/genetics ; Whole Genome Sequencing ; },
abstract = {The multidrug-resistant (MDR) Escherichia coli, particularly β-lactamase producing strains, has become a global health challenge, where wastewater systems, specially from hospitals, serve as critical reservoirs for the dissemination of resistance genes. The objectives of the study were to investigate the whole genome sequence diversity and genetic variations focusing on their evolutionary relationships, genetic similarity, and single nucleotide polymorphisms (SNPs) of pathogenic β-lactamase producing E. coli strains. A total of four β-lactamase producing E. coli strains, from differently located tertiary care hospitals, were included in this study. A heatmap of genetic similarity revealed near-identical genetic makeup among the strains. A number of genes including AcrAB-TolC, β-lactamases, and resistance determinants such as glpT, gyrA, msbA, and tet(M) were identified in these strains. However, the presence of virulence genes of the aerobactin synthesis gene (iucA, iutA) and type III secretion systems (espX1, espX4, espX5) in the strain has the potential for pathogenicity. These resistance genes were identified at the genomic level; however, their transcriptional expression was not evaluated and the detection of virulence-associated genes suggests that the isolates have the potential to cause disease and pathogenicity. These findings provide insights into the whole genome sequence diversity of E. coli in urban based tertiary care hospital wastewater, emphasizing the genetic variation and plasmid diversity in these E. coli strains, which may have implications in public health and microbial ecology of the environment.},
}

*Wastewater/microbiology
*Escherichia coli/genetics/isolation & purification/pathogenicity/classification
*Plasmids/genetics
*Genetic Variation
Hospitals
Polymorphism, Single Nucleotide
Phylogeny
Drug Resistance, Multiple, Bacterial/genetics
beta-Lactamases/genetics
Whole Genome Sequencing

@article {pmid42129938,
year = {2026},
author = {Zhao, L and Wu, L and Yin, S and Gao, W and Xiang, X and Xie, Y and Guo, Y and Wang, Z},
title = {Multi-omics reveals effects of several rumen bacteria on reproductive performance of sheep.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02426-5},
pmid = {42129938},
issn = {2049-2618},
support = {2025SNJF019//Three Agriculture Nine Party Science and Technology Cooperation Project/ ; 32573211//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Mounting evidence indicates that the rumen microbiota plays a crucial role in the reproductive health of sheep. However, the potential beneficial effects of rumen microbiota on lambing performance in sheep across different stages of the reproductive cycle and the precise mechanisms underlying these effects remain unclear. We aimed to elucidate the rumen microbial regulatory network underlying differences in reproductive performance in sheep by integrating multi-stage metagenomics and metabolomics.

RESULTS: No significant difference was observed in the ruminal microbial α-diversity between sheep with high and low litter size. However, significant stage-specific segregation was observed in their community structures. We identified a cohort of key species strongly associated with litter size. These included Asaia bogorensis, Methanolobus zinderi, Erwinia gerundensis, Marinobacter sp. BSs20148, and Lactobacillus amylolyticus enriched during pregnancy; Rhizobium gallicum, Aeromonas caviae, Pseudolysobacter antarcticus, Mucilaginibacter rubeus, Thermococcus paralvinellae, and Janthinobacterium svalbardensis enriched during lactation; Pseudomonas mandelii, Gordonia sp. HY186, Arachidicoccus sp. BS20, Mesotoga prima, Acidovorax ebreus, Donacia cinerea, and Salmonella enterica enriched during estrus. Host plasma metabolomics analysis further revealed an enrichment of a set of core metabolites in the blood of high-fertility sheep, including Inositol, 2-Linoleoylglycerol, lysophosphatidylcholines and neuromodulatory substances such as tyramine and sphingosine-1-phosphate. We constructed stage-specific "rumen microbe-rumen metabolite-plasma metabolite" regulatory axes. These results suggest the influence of the rumen microbiome on plasma metabolic profiles and subsequent fertility outcomes in sheep.

CONCLUSION: We elucidate the dynamic mechanism by which the rumen microbiota in high-fertility sheep is associated with superior reproductive performance through stage-adaptive community succession and functional remodeling, which in turn may modulate the host's neuroendocrine and lipid metabolic profiles. These findings provide a new perspective for understanding the regulation of fertility in ruminants and lay a theoretical foundation for improving reproductive efficiency through nutritional strategies targeting the rumen microbiota. Video Abstract.},
}

@article {pmid42129966,
year = {2026},
author = {LaRochelle, L and Morningstar, JL and Hoch, C and Rodriguez Materon, S and Hashioka, H and Scott, DJ and Gross, CE},
title = {Does Implanted Ankle Hardware Harbor Bacteria? Identification of the Microbial Profile Using Next-Generation DNA Sequencing? A Short Report.},
journal = {Foot & ankle international},
volume = {},
number = {},
pages = {10711007261438460},
doi = {10.1177/10711007261438460},
pmid = {42129966},
issn = {1944-7876},
abstract = {BackgroundNext-generation DNA sequencing (NGS) has improved detection of bacterial species and expanded understanding of the microbiome's influence on postoperative outcomes in orthopaedic patients. Although NGS has identified organisms linked to reoperations in shoulder surgery, its application in the foot and ankle remains unexplored. This study uses NGS to determine whether patients undergoing hardware removal exhibit a unique microbiome profile.Methods:A prospective study recruited 34 patients undergoing hardware removal surgery from the foot or ankle during 2020-2023. Patients were excluded based on any concern for infection prior to surgery. During the operation, the surgeon collected the removed hardware for analysis at a CLIA (Clinical Laboratory Improvement Amendments of 1988)-licensed molecular diagnostic laboratory. Majority of patients underwent surgery for painful orthopaedic hardware (70.6%). The cohort was predominantly female (62.2%) and mean age was 53.3 years (range 17-78). The mean time from primary implantation to hardware removal was 40.1 months (range 2.8-276.6 months).ResultsNGS identified bacterial DNA in 5 cases (14.7%), detecting 9 total organisms. Staphylococcus species were most common (44.4%), followed by Corynebacterium (22.2%). No significant associations were found between bacterial detection and patient demographics or with hardware removal performed for painful implants.Conclusion:This study found no consistent microbiome among patients undergoing hardware removal surgery, with Staphylococcus species being the most frequently detected organisms. These preliminary findings suggest that foot and ankle hardware does not consistently harbor bacteria detectable by NGS, although the small sample size limits generalizability and further investigation is warranted.},
}

@article {pmid42130174,
year = {2026},
author = {Pesenti, L and Lengrand, S and Kahn, A and Michot, L and Marchandise, F and Focant, C and Richet, S and Debode, F and Bragard, C},
title = {Xylem endophytes of Salicaceae: potential role in mitigating disease symptoms from Xylella fastidiosa or Brenneria salicis.},
journal = {The New phytologist},
volume = {},
number = {},
pages = {},
doi = {10.1111/nph.71230},
pmid = {42130174},
issn = {1469-8137},
support = {40006265//FRIA-FNRS/ ; },
abstract = {Increasing pressure from xylem-limited pathogens has driven the search for beneficial xylem-inhabiting endophytes that can enhance growth, stress tolerance, and disease resistance in woody plants. This study characterized the culturable xylem microbiota of Salicaceae species (willow and poplar) and evaluated their potential as biological control agents against vascular pathogens. A combination of microbial isolation, metabarcoding, and whole-genome sequencing was used to characterize xylem-associated bacteria. Functional traits were assessed through in vitro assays, while genome mining identified genes linked to plant-beneficial activities. Interactions between endophytes and pathogens were tested using fluorescently labeled strains in tobacco (Nicotiana tabacum) and in vitro-grown willow (Salix caprea). Bacterial genera (Bacillus, Pseudomonas, Erwinia) exhibited plant growth-promoting traits and strong antagonism against bacterial and fungal vascular pathogens, including Xylella fastidiosa, Brenneria salicis, Fusarium spp., and Verticillium dahliae. Genome analyses revealed functions related to nutrient acquisition, biofilm formation, and antimicrobial production. Co-inoculation assays significantly reduced pathogen load and disease symptoms in tobacco and mitigated symptoms in willow. Xylem endophytes act as context-dependent allies in woody plant defence. This study provides a functional and genomic framework supporting microbiome-based strategies to enhance resistance against vascular pathogens in long-lived woody hosts.},
}

@article {pmid42130196,
year = {2026},
author = {Cheng, X and Lei, Y and Zhang, S and Chen, L and Wang, Y},
title = {Butyrate Alleviates Hyperuricemia by Selectively Targeting the Metronidazole/Neomycin-Sensitive Bacterium Dubosiella newyorkensis.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c13934},
pmid = {42130196},
issn = {1520-5118},
abstract = {Hyperuricemia (HUA), a metabolic disorder resulting from disrupted uric acid (UA) homeostasis, is the principal etiological factor for gout. This study investigated the therapeutic potential of gut microbiota modulation in HUA using antibiotic-treated mouse models with butyrate intervention. Selective antibiotic screening identified the Dubosiella-type strain Dubosiella newyorkensis (Dn) as an effective intervention for HUA. Dn treatment significantly reduced UA production, improved renal function markers, and decreased oxidative stress. Dn enriches Bacteroides and Romboutsia while suppressing the pathobiont Thomasclavelia, thereby enhancing the production of acetate, propionate, and butyrate. Molecular analyses demonstrated that Dn downregulated the expression of URAT1 while upregulating ABCG2, thereby promoting UA excretion. Histopathological evaluation confirmed that Dn restored the glomerular atrophy, tubular dilation, and collagen deposition induced by HUA. These findings suggest that Dn is a promising multitarget therapeutic agent for HUA and provides a scientific foundation for the development of novel microbiome-based strategies against HUA.},
}

@article {pmid42130486,
year = {2026},
author = {Dichter, J},
title = {Fermented Dairy Products as Modulators of the Gut Microbiome: Greek Yogurt as a Model System.},
journal = {Food science & nutrition},
volume = {14},
number = {},
pages = {e71872},
pmid = {42130486},
issn = {2048-7177},
abstract = {Greek yogurt, characterized by its thick texture and higher protein content, contains reduced lactose levels while still preserving large colonies of active bacteria when compared to conventional (or "traditional") yogurt. The starter cultures listed on its label do more than just ferment milk; they actively reshape the gut microbiome and adjust host physiology. This review examines currently available observations about distinct bacterial types within this product, especially regarding its effects on intestinal balance. The ability to produce short-chain fatty acids is a property linked to these strains, along with the potential to stabilize gut lining function, adjust immunity patterns, aid blood sugar regulation, and even offer possible cardiovascular benefits. Greek yogurt's properties and potential differ from other fermented food items. Findings from experimental and clinical research suggest the lactic acid and Bifidobacterium species found in Greek yogurt contribute to increased microbiota variety, encourage growth of butyrate-producing bacteria, and strengthen the intestinal lining. Inflammation levels are reduced by these microbes, leading to greater lactose tolerance, smoother digestion, and balanced metabolic activity. Still, much of the available data is limited because most studies do not distinguish Greek yogurt from conventional yogurt in their analyses, even though differences exist in live cultures, survival through digestion, and manufacturing. Fermented vegetables may offer wider microbe variety; however, consistency in bacterial strains and stronger clinical evidence gives Greek yogurt significance in nutritional and microbiome research. Future investigations should focus on Greek yogurt and prioritize direct comparisons to other fermented foods. To credibly refine dietary recommendations, improved microbial methodologies and expanded trials among diverse populations are warranted.},
}

@article {pmid42130645,
year = {2026},
author = {Ali, N},
title = {Vitamin D Roles Across Developmental Stages in Pediatric Pneumonia: Linking Genetics, Microbiome, Maternal Status and Immunity.},
journal = {Health science reports},
volume = {9},
number = {},
pages = {e72520},
pmid = {42130645},
issn = {2398-8835},
abstract = {BACKGROUND: Pneumonia remains a leading cause of morbidity and mortality among children globally, especially in low- and middle-income countries, where poor nutrition and limited access to healthcare increase vulnerability. Vitamin D deficiency is common among children and has emerged as a significant risk factor associated with respiratory infections. This review aims to synthesize current evidence on the role of vitamin D across developmental stages in pediatric pneumonia.

METHODS: A comprehensive literature search was conducted in PubMed, Scopus, Web of Science, and Google Scholar to identify relevant studies on vitamin D and pediatric pneumonia. Peer-reviewed articles, including observational studies, randomized controlled trials, and reviews, were screened. Evidence was synthesized from immunology, genetics, maternal health, and microbiome research to provide an integrated perspective on vitamin D-mediated immune responses and clinical outcomes.

RESULTS: Mechanistically, vitamin D enhances host defense by inducing antimicrobial peptides such as cathelicidin and β-defensins. It improves macrophage phagocytic function, modulates Toll-like receptor signaling, and preserves airway epithelial barrier integrity. Vitamin D also modulates adaptive immunity by suppressing pro-inflammatory Th1 and Th17 responses while promoting regulatory T-cell activity and anti-inflammatory cytokine production. Epidemiological studies consistently show an association between low serum 25-hydroxyvitamin D levels and increased risk and severity of pneumonia, although results from supplementation trials remain heterogeneous. Recent evidence highlights additional modifiers of vitamin D-mediated immunity, including maternal vitamin D status, vitamin D receptor (VDR) genetic polymorphisms, early-life immune programming, and respiratory microbiome interactions, which may explain variability in clinical outcomes across populations and developmental stages.

CONCLUSION: Overall, this review provides a comprehensive framework linking vitamin D biology with immune system development in children and their risk of pneumonia. It emphasizes the importance of age-specific supplementation strategies and well-designed mechanistic and clinical studies to improve prevention and management.},
}

@article {pmid42130741,
year = {2026},
author = {Long, J and Zhao, J and Gu, X and Huang, C},
title = {Post-transplant diabetes mellitus after kidney transplantation: pathogenesis, risk factors, and management strategies.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1829579},
pmid = {42130741},
issn = {1664-2392},
mesh = {Humans ; *Kidney Transplantation/adverse effects ; Risk Factors ; *Postoperative Complications/etiology/therapy ; *Diabetes Mellitus/etiology/therapy ; Gastrointestinal Microbiome ; Immunosuppressive Agents/adverse effects ; },
abstract = {Post-transplant diabetes mellitus (PTDM) affects 7-39% of kidney transplant recipients and substantially worsens cardiovascular, infectious, and allograft outcomes. Although PTDM shares core pathophysiological features with type 2 diabetes-peripheral insulin resistance and impaired β-cell secretion-its etiology is fundamentally shaped by immunosuppressive therapy. Calcineurin inhibitors suppress insulin gene transcription via NFAT inhibition and exacerbate lipotoxicity; corticosteroids drive hepatic gluconeogenesis and impair GLUT4-mediated glucose uptake; and mTOR inhibitors reduce β-cell mass through mTORC1-dependent mechanisms. Chronic NF-κB/JNK-driven inflammation further amplifies insulin resistance and promotes β-cell apoptosis. Beyond these established mechanisms, we propose a unifying "gut-immune-metabolic axis" in which immunosuppression-induced gut microbiota dysbiosis-characterized by depletion of short-chain fatty acid-producing taxa (Roseburia, Faecalibacterium prausnitzii) and Akkermansia muciniphila-drives intestinal barrier dysfunction, endotoxemia, impaired FXR/TGR5-mediated GLP-1 secretion, and TMAO-associated metabolic inflammation, collectively perpetuating glucose dysregulation. Risk stratification integrates non-modifiable factors (advanced age, African American/Hispanic/South Asian ethnicity, TCF7L2 polymorphisms, autosomal dominant polycystic kidney disease) with modifiable determinants (pre-transplant dysglycemia, obesity, hypomagnesemia, hepatitis C and cytomegalovirus infections, acute rejection, and diuretic use). Diagnosis requires OGTT-centered assessment per the 2024 International Consensus guidelines, with cautious interpretation of HbA1c during the early post-transplant period. Management encompasses personalized immunosuppression (corticosteroid minimization, tacrolimus trough levels <10 ng/mL, and belatacept-based regimens in high-risk patients), structured lifestyle interventions, and emerging pharmacotherapies-particularly SGLT2 inhibitors and GLP-1 receptor agonists-which offer cardiometabolic benefits beyond glycemic control. Microbiome-targeted strategies, including prebiotics, probiotics, and fecal microbiota transplantation, represent a conceptually compelling frontier warranting prospective investigation. This framework reframes PTDM as a multi-hit, immunometabolic syndrome and provides a translational roadmap toward precision prevention and improved long-term transplant outcomes.},
}

Humans
*Kidney Transplantation/adverse effects
Risk Factors
*Postoperative Complications/etiology/therapy
*Diabetes Mellitus/etiology/therapy
Gastrointestinal Microbiome
Immunosuppressive Agents/adverse effects

@article {pmid42130766,
year = {2026},
author = {Li, Y and Sun, Y and Shi, L and Wang, A and Gao, X and Leng, H},
title = {The nasal-oral microbiome axis in allergic rhinitis: environmental triggers, microbial dysbiosis, and immune dysregulation.},
journal = {Frontiers in allergy},
volume = {7},
number = {},
pages = {1799085},
pmid = {42130766},
issn = {2673-6101},
abstract = {Allergic rhinitis (AR) is a common chronic inflammatory disease, which affects about 400 million people around the world. The role of the upper airway microbiota in the development of AR has recently emerged and seems to be an important player in its pathology, but there are still no detailed mechanistic models that incorporate exposure to the environment, dysbiosis of microbes or dysregulated immunity as a whole. In this review we summarize the state of the art about the microbiome nose-mouth connection in AR to understand how environmental stimuli change the microbiota composition as well as how an imbalance can induce allergy-related inflammation. This review follows a narrative approach. Literature was identified through systematic searches of PubMed, Web of Science, and Scopus databases (up to March 2025) using the following key terms and their combinations: "allergic rhinitis', "nasal microbiome", "oral microbiome", "dysbiosis", "epithelial barrier", 'short-chain fatty acids', "Th2 inflammation", and "probiotics". Inclusion criteria encompassed original research articles, systematic reviews, and meta-analyses published in English; conference abstracts, case reports, and purely non-human studies were excluded unless they provided mechanistic insights not available from human data. Environmental exposures substantially alter upper airway microbial communities. Air pollutants such as PM2.5 and diesel exhaust particles (DEP) damage epithelial tight junction proteins via reactive oxygen species (ROS), increasing nasal permeability. DEP additionally functions as an immune adjuvant by promoting pro-Th2 immune polarization. Antibiotic treatment during early childhood may affect GI tract development by altering resident bacterial populations, being considered as a strong risk factor for developing AR. On the other hand, farm exposure and microbial diversity provide protection by enhancing regulatory T cell induction. AR patients exhibit characteristic nasal dysbiosis, including overgrowth of Staphylococcus aureus and Moraxella catarrhalis alongside depletion of protective commensals such as Dolosigranulum pigrum and Corynebacterium spp. This dysbiosis disrupts the epithelial barrier, triggering alarmin release (TSLP, IL-25, IL-33) and amplifying type 2 inflammation. The oral microbiota also contributes via the oral-nasal-pulmonary axis whereby periodontal pathogens are pro-inflammatory while commensals have immunomodulatory roles. Mechanistically, microbiome-derived metabolites-especially short chain fatty acids and tryptophan derivatives-regulate the immune system via G protein-coupled receptors, histone deacetylase inhibition, and aryl hydrocarbon receptor activation. Dysbiosis promotes Th2 polarization, Treg/Th17 imbalance, and the activation of ILC2s, whereas neuro-immune interactions via TRPV1/TRPA1 enhance neurogenic inflammation. Translation to clinical opportunity: Microbiome based diagnostic biomarker; Probiotic (nasal/oral); Prebiotics; postbiotics, and engineered bacteria. Multi-omics based precision medicine using ML to stratify patient and tailor intervention. In summary, this review offers an insight into the theory of the microbiome-immunology interplay in AR as well as new avenues to consider regarding treatment of this condition through the nasal-oral microbiota axis.},
}

@article {pmid42130962,
year = {2026},
author = {Tomar, SS and Khairnar, K},
title = {Disruption in the Host-Phage Dynamics and Altered Microbial Diversity in the Upper Respiratory Tract of SARS-CoV-2-Infected Individuals.},
journal = {PHAGE (New Rochelle, N.Y.)},
volume = {7},
number = {1},
pages = {9-20},
pmid = {42130962},
issn = {2641-6549},
abstract = {BACKGROUND: The upper respiratory tract (URT) is an important site for the predisposition and multiplication of the SARS-CoV-2 virus. Therefore, URT is a critical site for investigating the changes in the microbiome caused by the SARS-CoV-2 infection. This study aims to compare phageome diversity and investigate the correlation of the phageome profiles with the sample type (SARS-CoV-2 or control) to determine the nature of phage-host interactions in the human URT microbiome and to assess the effect of SARS-CoV-2 viral load on host and phage abundance.

MATERIALS AND METHODS: In this study, we have used the whole-genome shotgun metagenomic approach to investigate URT swab samples (n = 96) collected from SARS-CoV-2-positive individuals (n = 48) (nonhospitalized but symptomatic) and healthy controls (n = 48) belonging to five districts of central India.

RESULTS: The results revealed distinct phageome profiles among the groups; Detrevirus dominated the composition in the control samples, while Maxrubnervirus was dominant in SARS-CoV-2 samples. Microbial diversity analysis showed significantly higher richness in the SARS-CoV-2 group compared to controls for both bacteria (Chao1: 886.00 vs. 351.00, p < 0.0001) and phages (Chao1: 39.00 vs. 16.00, p = 0.0002). Bacterial diversity (Simpson index) was lower in the SARS-CoV-2 group (0.88 vs. 0.93, p = 0.0024), whereas phage diversity was higher in the SARS-CoV-2 group (0.86 vs. 0.79, p = 0.0384). Viral load, as reflected by cycle threshold (Ct) values, significantly influenced both bacteria (H = 6.69, p = 0.035) and phage (H = 8.97, p = 0.011) abundances. Host-phage interaction networks appeared disrupted in SARS-CoV-2 samples, with a weaker logistic model fit (R [2] = 0.7425) than controls (R [2] = 0.9265).

CONCLUSION: SARS-CoV-2 infection alters URT microbiome composition, increasing microbial diversity but disrupting host-phage dynamics. SARS-CoV-2 Viral load correlates with the shifts in microbial abundance, indicating infection-driven shifts in microbiome stability compared to healthy controls.},
}

@article {pmid42131067,
year = {2026},
author = {Glynn, TR and Broedlow, CA and Rodriguez, V and Nogueira, NF and Londono, V and Brophy, T and Pallikkuth, S and Roach, M and Pahwa, S and Fein, LA and Hurwitz, BE and Jones, D and Alcaide, ML and Klatt, N and Martinez, C},
title = {Microbiota, Gender-Affirming Hormone Therapy, and Inflammatory Biomarkers in Transgender Women with HIV: Potential Implications for Cardiovascular Disease.},
journal = {Transgender health},
volume = {11},
number = {2},
pages = {114-125},
pmid = {42131067},
issn = {2688-4887},
support = {T32 AI007433/AI/NIAID NIH HHS/United States ; },
abstract = {PURPOSE: The intersecting disparities of human immunodeficiency virus (HIV) and cardiovascular disease (CVD) among transgender women have raised questions about the role of the gut microbiota and gender-affirming hormone therapy (GAHT) in the pathogenesis of CVD in the context of HIV. The purpose of this study was to provide an early exploration of the associations between these possible mechanisms driving inflammatory CVD risk markers among transgender women with HIV.

METHODS: We conducted a preliminary study with 21 transgender women with HIV exploring the relationship between GAHT use (self-report), gut/rectal microbiota composition (rectal swabs), and inflammatory markers linked to CVD (plasma). Microbiota measures included alpha (richness, evenness, and Shannon diversity) and beta (Bray-Curtis, un/weighted UniFrac) diversity metrics. Inflammatory biomarkers included intestinal fatty-acid binding protein, monocyte chemoattractant protein-1, soluble CD163, intercellular adhesion molecule 1, tumor necrosis factor alpha (TNFa), soluble TNF receptor I (sTNF-I), sTNF-II, interleukin (IL)-6, IL-8, IL-1b, IL-1a, soluble CD14, d-dimer (domain dimer), vascular cell adhesion molecule 1, and high-sensitivity C-reactive protein. Wilcoxon rank sum test, log-level regression, Spearman's rho, permutational multivariate analysis of variance, and differential abundance testing assessed relationships between constructs.

RESULTS: Key inflammatory markers linked to CVD were associated with GAHT use-an increased sTNF-I and sTNF-II levels and decreased IL-1a levels. Microbiota composition was not related to GAHT use but was variably associated with inflammatory biomarkers related to CVD risk.

CONCLUSIONS: Although preliminary, these findings suggest a potential association between inflammation linked to CVD risk and microbiota composition and GAHT. The results contribute to the characterization of interconnecting factors that may inform understanding and interventions to enhance overall health and well-being in transgender women with HIV. Further research is essential to elucidate the mechanisms underlying these associations, ultimately striving for health equity.},
}

@article {pmid42131202,
year = {2026},
author = {Sivamaruthi, BS and Kesika, P and Chaiyasut, C and Ragu Varman, D},
title = {Microbiome driven modulation of neurotransmitters: implications for neurotransmission and mood disorders.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1750377},
pmid = {42131202},
issn = {1664-302X},
abstract = {The human gut microbiome has emerged as a crucial regulator of neurophysiological processes by engaging with the central nervous system (CNS) via the microbiota-gut-brain (MGB) axis. One of the most significant ways gut microorganisms influence brain functions is by altering the levels of neurotransmitters. A significant relationship exists between microbial activity and mood, behavior, and cognition. Gut microorganisms can make or break down bioactive substances like serotonin, dopamine, γ-aminobutyric acid (GABA), glutamate, acetylcholine, and histamine. These microbial modulations influence precursor availability, receptor sensitivity, synaptic signaling dynamics, and neuroimmune modulation, thereby indirectly shaping neurotransmission within central circuits. These neurochemical effects, particularly involving serotonergic, dopaminergic, GABAergic, and glutamatergic pathways, are mediated through microbial metabolites such as short-chain fatty acids (SCFAs), alterations in tryptophan metabolism, immune system activation, vagal nerve transmission, and the control of the hypothalamic-pituitary-adrenal (HPA) axis. Changes in the composition of the microbiome have been frequently linked to mood disorders, such as depression, anxiety, bipolar disorder, and schizophrenia. The current review integrates findings from preclinical and clinical studies on microbiome-related neurotransmitter modulation, emphasizing novel therapeutics such as probiotics, prebiotics, fecal microbiota transplantation, and dietary alterations. Unlike previous reviews that primarily focus on microbiome composition or therapeutic interventions such as probiotics and fecal microbiota transplantation, this review adopts a neurotransmitter-centered framework, integrating microbial regulation of serotonergic, dopaminergic, GABAergic, glutamatergic, cholinergic, and histaminergic systems with the pathophysiology of mood disorders. Connecting microbiota-driven modulation of neurochemistry to mental outcomes offers a promising adjunctive avenue for mood disorder management, pending rigorous mechanistic and clinical validation.},
}

@article {pmid42131203,
year = {2026},
author = {Zahra, M and Ouf, A and Azzazy, HME and Moustafa, A},
title = {Metagenomic profiling of gut microbiome signatures across liver disease stages and HCV-related hepatocellular carcinoma in Egyptian patients.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1758563},
pmid = {42131203},
issn = {1664-302X},
abstract = {INTRODUCTION: Dysbiosis in the gut microbiome, particularly concerning the synchronous crosstalk between the gut and the liver, has been associated with various diseases. This study examines the gut microbiome's role in liver diseases among Egyptian patients, with a focus on the hepatitis C virus (HCV) and hepatocellular carcinoma (HCC), both of which are highly prevalent in Egypt.

METHODS: Utilizing shotgun metagenomic sequencing, we analyzed microbial gene catalogs and taxonomic profiles from 46 Egyptian patients categorized into five groups: healthy individuals, liver disease patients of different etiologies, post-HCV, treated HCV, and HCV-HCC patients.

RESULTS: Healthy and treated HCV patients exhibited distinct microbial profiles characterized by an abundance of beneficial bacteria, Faecalibacterium and Bifidobacterium (p < 0.05), associated with anti-inflammatory short-chain fatty acid production. Conversely, liver disease and HCC patients displayed increased pathogenic bacteria, Escherichia (p < 0.05), and genes linked to inflammation and oncogenesis, including lipopolysaccharide biosynthesis.

DISCUSSION: These findings suggest a dominance of Faecalibacterium in healthy Egyptians, likely attributable to traditional dietary patterns, and cytochrome P450 genes as potential HCC biomarkers, possibly connected to aflatoxin exposure. Treated HCV patients showed significant microbiome recovery, reflecting effective antiviral therapy. These findings emphasize that Egypt-specific factors, such as persistent resistance genes post-HCV due to antibiotic use and the prominence of bile acid metabolism genes, are influenced by high HCV prevalence and environmental exposures like aflatoxins. Taken together, the results highlight the need for region-specific microbiome research priorities in Egypt and underscore how local dietary, clinical, and environmental factors may shape future objectives in understanding liver disease pathogenesis and prevention.},
}

@article {pmid42131238,
year = {2026},
author = {Alblaji, M},
title = {Plant-based diets for human health with implications for cardiometabolic health, gut microbiome, and nutritional adequacy.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1830797},
pmid = {42131238},
issn = {2296-861X},
abstract = {Plant-based diets have gained considerable interest in recent times due to their perceived health and environmental benefits. However, the term "plant-based diet" refers to a broad range of diets with a wide range of differences in food quality and nutritional content. This article aims to summarize the available evidence regarding the health and environmental impacts of plant-based diets, including new trends and issues. Epidemiological studies, RCTs, and life cycle assessment studies were searched in various scientific databases to investigate the relationship between plant-based diets and various health outcomes or environmental impacts. Available evidence from prospective studies and RCTs suggests that well-planned plant-based diets are associated with a lower risk of cardiometabolic diseases and beneficial alterations in the gut microbiome. Environmental studies have uniformly found lower greenhouse gas emissions, land use, and water use associated with a human diet compared with an animal-based diet; however, the extent of these positive impacts depends on the diet composition. On the other hand, nutrient adequacy such as iron, vitamin B12, omega-3 fatty acids, processing, and socio-economic factors are also important considerations. This review aims at an integrated approach in environmental sustainability viewpoints with health results, comprehensive understanding the relationship between the quality of diet and health outcomes in the context of a circular food system and research priorities in guiding future diets.},
}

@article {pmid42131305,
year = {2026},
author = {Toto, F and Cardile, S and Scanu, M and Marzano, V and Petito, V and Masi, L and Puca, P and Giorgio, V and Alterio, T and Diamanti, A and De Angelis, P and Lopetuso, LR and Scaldaferri, F and Putignani, L and Del Chierico, F},
title = {Ecological patterns of the gut mycobiome and microbiome in ulcerative colitis across life stages.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1769892},
pmid = {42131305},
issn = {2235-2988},
mesh = {Humans ; *Colitis, Ulcerative/microbiology/immunology ; *Mycobiome ; *Gastrointestinal Microbiome ; Adult ; Child ; Male ; Female ; *Fungi/classification/genetics/isolation & purification ; Bacteria/classification/genetics/isolation & purification ; Middle Aged ; Young Adult ; Adolescent ; Dysbiosis/microbiology ; Metagenome ; Child, Preschool ; Age Factors ; Aged ; Feces/microbiology ; },
abstract = {INTRODUCTION: Age-related variations in the gut microbial communities may influence immune regulation and inflammatory processes in inflammatory bowel diseases (IBD). However, distinguishing age effects from differences in clinical characteristics remains challenging.

METHODS: We investigated life-stage-associated patterns of the gut microbiome and mycobiome while accounting for clinical heterogeneity between paediatric and adult ulcerative colitis (UC) populations. We analysed 73 targeted metagenomes of bacteria and 69 targeted metagenomes of fungi from 26 paediatric and 47 adult patients with UC. Microbial diversity metrics and multivariate analyses were applied to evaluate community variation, and mucosal immune markers were assessed by ELISA. Clinical variables, including disease activity, duration, and treatment exposure, were considered when interpreting age-related microbial differences.

RESULTS: Fungal communities exhibited higher richness in adults and formed distinct age-related clusters in beta-diversity analyses, whereas bacterial composition remained largely comparable across age groups. Children were enriched in inflammation-associated fungi (Saccharomycetes, Aureobasidium, Cladosporium) and depleted in taxa commonly linked to gut health (Clavispora, Vishniacozyma, Betamyces). Stratification by life stage identified young adults as displaying the most pronounced dysbiosis, characterised by Basidiomycota/Ascomycota and Firmicutes/Bacteroidota ratios, and reduced Faecalibacterium prausnitzii abundance. Age-associated immune patterns were observed, with lysozyme levels increasing across life stages, correlating with sIgA, and positively associating with F. prausnitzii, although declining with increasing disease severity.

DISCUSSION: Age-related variation was more evident in fungal than bacterial communities, suggesting that host developmental and immunological factors contribute to mycobiome configuration beyond clinical imbalance alone. Together, these findings indicate that life stage is linked to ecological variation of the gut mycobiome and mucosal immune responses in UC, while bacterial communities appear primarily shaped by disease-related factors. The transition from childhood to adulthood may represent a critical window of host-fungal interaction relevant for age-tailored microbiome-based strategies.},
}

Humans
*Colitis, Ulcerative/microbiology/immunology
*Mycobiome
*Gastrointestinal Microbiome
Adult
Child
Male
Female
*Fungi/classification/genetics/isolation & purification
Bacteria/classification/genetics/isolation & purification
Middle Aged
Young Adult
Adolescent
Dysbiosis/microbiology
Metagenome
Child, Preschool
Age Factors
Aged
Feces/microbiology

@article {pmid42131426,
year = {2026},
author = {Hong, HH and Kim, TH and Kim, D and Kim, J and Jo, Y and Park, Y and Jeong, E and Lee, N and Roh, H and Jang, H and Kim, SM},
title = {A pilot study on microbial dynamics in drainage fluid during trauma recovery.},
journal = {Annals of surgical treatment and research},
volume = {110},
number = {5},
pages = {347-358},
pmid = {42131426},
issn = {2288-6575},
abstract = {PURPOSE: Drainage fluid may serve as a biologically informative indicator of immune and infectious status during postsurgical recovery after trauma. However, microbiome shifts in drainage fluid associated with clinical resilience have not yet been characterized. This study aimed to investigate microbial dynamics in drainage fluid across the intensive care unit (ICU) and ward recovery phases in Korean trauma patients.

METHODS: A total of 25 drainage and 10 stool samples were collected from 10 trauma patients who underwent abdominal surgery at a regional trauma center. Microbial composition was analyzed using 16S ribosomal RNA amplicon sequencing. Alpha and beta diversity were compared between sample types and recovery stages. Linear mixed-effects models were used to identify recovery-associated taxa while adjusting for clinical variables, and predicted metabolic pathways were assessed using PICRUSt2.

RESULTS: Drainage fluid harbored distinct microbial communities independent of the intestinal microbiota. Shared taxa between drainage and stool increased significantly in patients with bowel injury, suggesting microbial translocation. Seven genera and 5 species showed significantly decreased abundance during the ward stage, with Modestobacter and Blastococcus tunisiensis demonstrating the highest discriminative ability between recovery stages (area under the curve = 0.721). Predicted metabolic pathways related to fatty acid degradation, amino acid degradation, and pro-inflammatory processes were more active during the ICU stage.

CONCLUSION: These findings provide preliminary evidence that drainage fluid microbiome profiles may reflect recovery dynamics following trauma, supporting its potential utility for microbiome-based monitoring and biomarker discovery in trauma surgery.},
}

@article {pmid42131433,
year = {2026},
author = {Salamon, A and Bel Rhali, S and Szabó, A and Miklósi, Á and Andics, A and Felföldi, T and Gácsi, M and Kubinyi, E},
title = {Nasal microbiota profiles are similar at two swabbing depths in healthy awake dogs.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1795324},
pmid = {42131433},
issn = {2297-1769},
abstract = {The nasal microbiome may play an important role in dogs' olfaction, as microbial communities in the nasal cavity can directly interact with the olfactory epithelium. Previous studies have used various sampling methods and depths to examine the canine nasal microbiota and the effect of sampling depth on the detected nasal microbiota remains unclear. To address this, we investigated and compared the nasal microbiota of 81 awake family dogs, sampled at two swabbing depths (15 mm and 25 mm) of the left nostril in the same individuals. The most abundant bacterial taxa in our nasal samples belonged to Moraxella (Gammaproteobacteria), consistent with previous studies. The 15 mm samples had a higher Shannon Diversity Index compared to the 25 mm samples, indicating closer proximity to the external environment. However, we found no significant differences in richness and overall microbiota composition between the two sampling depths. These results indicate that bacterial community profiles within the anterior nasal cavity are similar at the two examined depths. Because the deeper sample was always collected first from the same nostril, potential order effects cannot be excluded. Nevertheless, based on the findings, we recommend using a sampling depth up to 15 mm when examining the nasal microbiota of healthy awake mesocephalic dogs in field settings, as it is less invasive and minimises discomfort.},
}

@article {pmid42131446,
year = {2026},
author = {Heasley, CK and Stefanova, V and Funk, C and Freitas, AC and Li, G and Pell, LG and Bassani, DG and O'Callaghan, KM and Shah, PS and Shawon, J and Gaffar, SMA and Haque, R and Sarker, SA and Roth, DE},
title = {Neonatal faecal abundance of Bifidobacterium longum subspecies infantis is not associated with anthropometric outcomes up to 6 months of age in Bangladeshi infants.},
journal = {Gut microbiome (Cambridge, England)},
volume = {7},
number = {},
pages = {e5},
pmid = {42131446},
issn = {2632-2897},
abstract = {B. infantis abundance in the infant gut may be associated with growth and health outcomes. However, these relationships have not been widely studied in settings where B. infantis is a dominant early-life commensal and growth faltering is prevalent. Here, we estimated associations between neonatal B. infantis abundance and anthropometric outcomes up to 6 months of age in generally healthy infants in Dhaka, Bangladesh; diarrhoea and hospitalizations (at 1-2 and 6 months) were secondary morbidity outcomes. B. infantis stool absolute abundance was quantified by qPCR; for each infant, the primary exposure was mean abundance (0-28 days). Length-for-age, weight-for-age, and weight-for-length z-scores were derived at birth, 2, 3, and 6 months. Neonatal B. infantis abundance had a bimodal distribution, with 63% of infants having detectable B. infantis by 28 days of age. Anthropometric z-score distributions were shifted down, with means below zero. Neonatal B. infantis abundance was not associated with any anthropometric outcome at 2, 3, or 6 months of age (n = 830), or with the risks of diarrhoea or hospitalizations. The lack of association of neonatal B. infantis abundance with growth outcomes suggests that promoting early B. infantis colonization is unlikely to improve growth in populations with postnatal faltering.},
}

@article {pmid42131447,
year = {2026},
author = {Chia Liu, T and Rojas-Velazquez, D and Kidwai, S and Hogenkamp, A and Garssen, J and Kraneveld, AD and Lopez-Rincon, A},
title = {Machine learning identifies differences between breast milk and formula in the gut microbiome.},
journal = {Gut microbiome (Cambridge, England)},
volume = {7},
number = {},
pages = {e7},
pmid = {42131447},
issn = {2632-2897},
abstract = {In this study, we analysed differences in the infant gut microbiome between breastfed and formula-fed infants using novel machine learning techniques. Breast milk, rich in bioactive agents, supports microbiota composition and immune development, while formulas aim to replicate its nutritional profile. We applied a methodology combining the DADA2 pipeline for 16S rRNA sequencing with the Recursive Ensemble Feature Selection (REFS) algorithm for biomarker discovery. We analysed three publicly available 16S rRNA datasets: PRJNA633365 (70 stool samples from China), PRJDB7295 (40 stool samples from the Philippines), and PRJNA562650 (40 stool samples from China). The discovery dataset (PRJNA633365) revealed 16 significant taxa out of 1,227, validated across the other two datasets. Next, we compared REFS performance with another feature selection algorithm, SelectKBest. Finally, we conducted a literature review to explore links between identified taxa and medical conditions. Additionally, we used MicrobiomeAnalyst to examine associations with diseases, diet, and lifestyle. Our results show differences in the bacterial composition between breastfed and formula-fed infants, and these findings were validated in two independent datasets. Future research should explore the functional roles of these taxa and consider regional and dietary variability to enhance understanding of microbiome dynamics and long-term health outcomes.},
}

@article {pmid42131482,
year = {2026},
author = {Udobi, ME and Bella-Omunagbe, M and Afolabi, IS and Chinedu, SN},
title = {Bioactive compounds as therapeutic modulators of metabolic syndrome: targeting inflammation and gut microbiota regulation.},
journal = {Frontiers in physiology},
volume = {17},
number = {},
pages = {1766078},
pmid = {42131482},
issn = {1664-042X},
abstract = {Food bioactives, including polyphenols, flavonoids, omega-3 fatty acids, and glucosinolates, play a crucial role in preventing metabolic syndrome by modulating chronic inflammation, gut microbiota homeostasis, and metabolic processes. These compounds influence key molecular pathways implicated in metabolic dysfunction and systemic inflammation. This review explores the mechanisms through which food bioactives contribute to metabolic health, emphasizing their role in inflammation regulation, gut microbiota modulation, and insulin sensitivity. A comprehensive literature review was conducted using databases such as PubMed, Scopus, and Web of Science. Relevant peer-reviewed articles, meta-analyses, and clinical trials published in the last two decades were analyzed, focusing on bioactives' biochemical actions and therapeutic potential in Metabolic syndrome. The study showed that bioactives mitigate inflammation by inhibiting NF-κB signaling and NLRP3 inflammasome activation, reducing pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). They also modulate gut microbiota, promoting beneficial bacteria (e.g., Akkermansia muciniphila) and enhancing gut barrier integrity via increased expression of tight junction proteins. Short-chain fatty acids (SCFAs) derived from microbial metabolism contribute to systemic anti-inflammatory effects. Clinical studies indicate that polyphenol-rich diets, such as the Mediterranean diet, improve metabolic syndrome parameters by lowering inflammatory markers, enhancing lipid profiles, and improving insulin sensitivity. Despite promising findings, challenges such as poor bioavailability and variability in gut microbiome responses hinder clinical application. Strategies like nanoencapsulation and microbiome-targeted nutrition may optimize bioactive efficacy. Overall, food bioactives represent a promising strategy for metabolic health. Future research should focus on enhancing bioavailability, personalized nutrition, and large-scale clinical trials to establish optimal dosing and long-term benefits.},
}

@article {pmid42131744,
year = {2026},
author = {Ogedengbe, O and Hunt, J and Pang, A and Gupta, D},
title = {Silicon-mediated drought resilience mechanisms in crops: from physiology to molecular insights.},
journal = {Frontiers in plant science},
volume = {17},
number = {},
pages = {1788106},
pmid = {42131744},
issn = {1664-462X},
abstract = {Drought stress increasingly constrains crop growth, yield, and quality through reduced photosynthesis, impaired nutrient uptake, and oxidative damage, with recent occurrences causing substantial yield losses across major production regions. Silicon (Si), although not an essential nutrient, is a prevalent, non-toxic, "quasi-essential" element that can enhance crop performance under water limitation; however, Si-induced drought-mitigation mechanisms are frequently reported in isolation, based on individual studies. This review aims to provide a holistic understanding of Si's role in enhancing plant resilience to water stress by comprehensively compiling and integrating physiological to molecular mechanisms underpinning Si-mediated drought resilience, while contextualising soil Si availability, plant uptake and accumulation diversity, and agronomic delivery options. Across crops, Si fertilisation consistently improves water relations by promoting root growth, hydraulic conductance, and aquaporin regulation, enabling osmotic adjustment and modulating stomatal behaviour through hormone-reactive oxygen species interactions. Evidence is synthesised from controlled and field studies, alongside temporal trend analyses showing a shift from uptake/transport research (pre-2010) to physiological characterisation (2010-2015), and to integrative multi-omics (2020-present), including transcriptomics and metabolomics. Key research gaps include limited field validation, inconsistent experimental designs and drought imposition protocols, incomplete multi-omics-to-trait integration, and underexplored Si-microbiome interactions. Optimising the Si source, dosage, timing, and application method across different species and environments presents a practical approach to developing climate-resilient, low-input cropping systems in the face of increasing drought risk.},
}

@article {pmid42131794,
year = {2026},
author = {Kalin, K and Rådholm, K and Olsson, L and Tremaroli, V and Woodward, M and Wennberg, M and Bäckhed, F and Rolandsson, O},
title = {Effects of saccharin on insulin sensitivity in adult, overweight individuals without diabetes: a real-world pilot study.},
journal = {Journal of the Endocrine Society},
volume = {10},
number = {6},
pages = {bvag096},
pmid = {42131794},
issn = {2472-1972},
abstract = {CONTEXT: It has been suggested that consumption of saccharin, a widely used artificial sweetener, decreases insulin sensitivity in rodents and humans, but studies show conflicting results.

OBJECTIVE: To investigate if saccharin affects insulin sensitivity in a proof-of-concept study in humans using hyperinsulinemic-euglycemic clamp.

METHODS: In an open-label pilot study, we recruited 14 overweight participants without diabetes who were mean 60.5 (SD 4.1) years of age and had a body mass index of 27.6 (SD 0.7). Insulin sensitivity, assessed by hyperinsulinemic-euglycemic clamp, was determined before and after consumption of 5 mg/kg saccharin/day for 3 months. Blood was collected for analysis of diabetes-related biomarkers. Stool samples were collected before, during, and after saccharin consumption for microbiota profiling by 16S rRNA gene sequencing.

RESULTS: Thirteen of the 14 participants (6 men, 7 women) completed the study. There was no change in insulin sensitivity (mean M value difference [ΔM] -0.1, P = .85) or body weight (mean difference -0.1 kg, P = .70) after consumption of saccharin. However, the mean glycated hemoglobin decreased from 38.7 mmol/mol (SD 3.0) at visit 1 to 36.8 (SD 3.4) at visit 4 (P = .003). Overall, there was no change in composition or richness of the gut microbiota at the end of the study.

CONCLUSION: This study did not demonstrate an association between saccharin intake and impaired insulin sensitivity in adult, overweight participants without diabetes assessed by hyperinsulinemic-euglycemic clamp.},
}

@article {pmid42132027,
year = {2026},
author = {Osakunor, DNM and Pfavayi, LT and Mduluza, T and Mutapi, F},
title = {Schistosomiasis and stunting: microbial and metabolic mechanisms in early childhood.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1950},
pages = {},
doi = {10.1098/rstb.2025.0094},
pmid = {42132027},
issn = {1471-2970},
support = {/AMS_/Academy of Medical Sciences/United Kingdom ; //Thrasher Research Fund/ ; //British Academy/ ; //Royal Society/ ; },
mesh = {Humans ; Child, Preschool ; *Growth Disorders/parasitology/etiology/epidemiology ; *Gastrointestinal Microbiome ; Zimbabwe/epidemiology ; *Schistosomiasis haematobia/complications/drug therapy/epidemiology/parasitology ; Schistosoma haematobium/physiology ; Infant ; Praziquantel/therapeutic use ; Animals ; },
abstract = {Stunting (low height-for-age > 2 s.d. below the WHO child growth standards median) is a key indicator of chronic malnutrition and is influenced by poor nutrition, infections, chronic inflammation and impaired gut health. In sub-Saharan Africa, stunting frequently occurs in regions where schistosomiasis is endemic. Our previous research in Zimbabwean preschool children (≤ 5 years) found that Schistosoma haematobium infection alone could account for up to one-third of stunting cases. Using epidemiological, gut microbiome and metabolomic analyses, we investigated how this parasitic infection contributes to poor growth. Infected children showed significantly altered gut microbiome profiles compared to uninfected peers, indicating potential microbiome disruption linked to disease and impaired development. Metabolomic profiling revealed that S. haematobium infection elevated energy- and purine-related metabolites, reflecting metabolic stress associated with malnutrition. Early treatment with praziquantel did not significantly alter the microbiome but did restore normal metabolic profiles, aligning with observed catch-up growth. Here, we synthesize findings from our studies and others to highlight opportunities for intervention and key research gaps, supporting the inclusion of praziquantel in early health programmes and integrated strategies combining treatment with nutrition. Further research, particularly longitudinal studies, is needed to confirm causality and optimize child health outcomes in endemic areas. This article is part of the theme issue 'Biological, biomedical and environmental drivers of stunting'.},
}

Humans
Child, Preschool
*Growth Disorders/parasitology/etiology/epidemiology
*Gastrointestinal Microbiome
Zimbabwe/epidemiology
*Schistosomiasis haematobia/complications/drug therapy/epidemiology/parasitology
Schistosoma haematobium/physiology
Infant
Praziquantel/therapeutic use
Animals

@article {pmid42132029,
year = {2026},
author = {Mweetwa, MN and Ashan, K and Kung, V and McNulty, NP and Besa, E and Barratt, MJ and Posma, J and Amadi, B and Gordon, JI and Kelly, P},
title = {Small intestinal microbiota in Zambian children with stunting and severe acute malnutrition.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1950},
pages = {},
doi = {10.1098/rstb.20250088},
pmid = {42132029},
issn = {1471-2970},
support = {/MRC_/Medical Research Council/United Kingdom ; //Bill and Melinda Gates Foundation/ ; },
mesh = {Humans ; Zambia ; *Gastrointestinal Microbiome ; *Growth Disorders/microbiology/epidemiology ; *Severe Acute Malnutrition/microbiology/epidemiology ; Infant ; Child, Preschool ; RNA, Ribosomal, 16S/analysis ; *Bacteria/classification/isolation & purification/genetics ; Male ; Female ; *Intestine, Small/microbiology ; *Duodenum/microbiology ; },
abstract = {Childhood malnutrition is linked to gut microbiome changes; however, most studies focus on faecal samples, while less is known about the small intestinal microbiome. Here, we characterized the duodenal microbiota of children in Zambia with severe acute malnutrition (SAM) and stunting and compared the microbiomes of stunted children living across the globe. To do this, duodenal aspirates from only stunted (i.e. not concurrently wasted) (n = 53) and SAM (n = 24) Zambian children were analysed by 16S rRNA gene amplicon sequencing. Associations between bacterial composition, clinical features and biomarkers of enteropathy were explored. Comparison of duodenal 16S rRNA gene datasets from malnourished children in different countries was also performed using publicly available datasets to assess the impact of age and geography on microbial diversity and composition. The duodenal microbiota in both stunted and SAM children was dominated by Streptococcus, Granulicatella, Gemella and Klebsiella. Children with SAM had lower α-diversity than stunted children. Meta-analysis revealed similarities in the bacterial composition of age-matched children in different countries, but relative abundances and their association with nutritional status differed. This study offers insight into the duodenal microbiota in children with different states of malnutrition, highlighting the potential influence of geography and age in shaping the proximal small intestine. This article is part of the theme issue 'Biological, biomedical and environmental drivers of stunting'.},
}

Humans
Zambia
*Gastrointestinal Microbiome
*Growth Disorders/microbiology/epidemiology
*Severe Acute Malnutrition/microbiology/epidemiology
Infant
Child, Preschool
RNA, Ribosomal, 16S/analysis
*Bacteria/classification/isolation & purification/genetics
Male
Female
*Intestine, Small/microbiology
*Duodenum/microbiology

@article {pmid42132030,
year = {2026},
author = {Mweetwa, MN and Kelly, P and Posma, J},
title = {A meta-analysis of gut microbiome research in malnourished African populations: a natural language processing approach.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1950},
pages = {},
doi = {10.1098/rstb.2025.0038},
pmid = {42132030},
issn = {1471-2970},
support = {/MRC_/Medical Research Council/United Kingdom ; },
mesh = {*Gastrointestinal Microbiome ; Humans ; *Natural Language Processing ; Africa South of the Sahara/epidemiology ; *Malnutrition/microbiology ; *Child Nutrition Disorders/microbiology ; },
abstract = {Malnutrition still affects millions of children in Africa. Changes in the gut microbiome have been implicated in malnutrition, but there has been inconsistent nomenclature of microbes. This meta-analysis reviews the microbiome literature using natural language processing (NLP) methods. We searched PubMed for gut microbiome studies of undernourished children living in low- and middle-income countries (LMICs). The primary analysis focused on continental coverage and study characteristics of microbiome research in sub-Saharan Africa (ss-Africa). We also used an NLP tool for normalizing primary data from full-text publications in ss-Africa compared with other LMICs, and between diseased and healthy children. We identified 16 studies. Most studies were conducted in Malawi and characterized the faecal microbiome using 16S rRNA sequencing. For comparison, 18 studies conducted in Bangladesh, India, Pakistan and Peru were included. With this, we identified frequently reported microbes that were distinctly identified in ss-Africa and highlighted possible signatures of an undernourished faecal microbiome across the globe. The consistent associations between elevated Pseudomonadota levels and severe acute malnutrition provide new insights into host-microbiome interactions in African contexts. However, the overlap between taxa associated with healthy and stunting underscores the need for further research to better inform potential targeted interventions in Africa. This article is part of the theme issue 'Biological, biomedical and environmental drivers of stunting'.},
}

*Gastrointestinal Microbiome
Humans
*Natural Language Processing
Africa South of the Sahara/epidemiology
*Malnutrition/microbiology
*Child Nutrition Disorders/microbiology

@article {pmid42132032,
year = {2026},
author = {Hlongwa, N and Rich, K and Kelly, P and Ngobeni-Nyambi, R and Stone, W and von Fintel, M and Schenck, C and Swart, R and Makhalanyane, T and Burger, R},
title = {The physiology of poverty: gut microbiome and pathways to child stunting.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1950},
pages = {},
doi = {10.1098/rstb.2025.0034},
pmid = {42132032},
issn = {1471-2970},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Growth Disorders/etiology/microbiology ; *Poverty ; Hygiene ; Child, Preschool ; Child ; },
abstract = {The causes of childhood stunting remain debated, with emerging evidence highlighting the complexity of poverty-related mechanisms. While nutrition, healthcare and sanitation have traditionally been viewed as the primary drivers of stunting, new research highlights the physiological mediators linking poverty to impaired growth. Chronic exposure to unsanitary environments may lead to environmental enteric dysfunction, a subclinical gut condition that may impair the development of the gut microbiome. Stunted children frequently exhibit an immature and dysbiotic gut microbiome, which is linked to higher levels of gut inflammation, reduced nutrient assimilation and increased susceptibility to infections. Here, we examine how poverty-related factors, including poor diet and hygiene, affect gut health and early neurodevelopment, with a particular focus on the gut-brain axis. Understanding this 'physiology of poverty' reveals that effective interventions must extend beyond food provision to integrate improvements in water, sanitation, hygiene (WASH) and microbiome support (e.g. via probiotics or prebiotics). A holistic strategy targeting environmental and biological factors in early life is critical to disrupting the intergenerational cycle of stunting and poverty. We identify key evidence gaps and stress the need for multidisciplinary, context-specific approaches to mitigate stunting's long-term association with health and human capital. This article is part of the theme issue 'Biological, biomedical and environmental drivers of stunting'.},
}

Humans
*Gastrointestinal Microbiome
*Growth Disorders/etiology/microbiology
*Poverty
Hygiene
Child, Preschool
Child

@article {pmid42132035,
year = {2026},
author = {Htet, MK and Nurfadilah, M and Ramsteijn, AS and Angelin, TC and Ameline, AS and Momo Kadia, B and Gabain, IL and Davies-Kershaw, H and Calvo-Urbano, B and Webster, JP and Ferguson, EL and Allen, S and Walker, AW and Fahmida, U},
title = {Exploring the diet-microbiome-growth axis among under-2-year-old children: a case-control study in East Lombok, Indonesia.},
journal = {Philosophical transactions of the Royal Society of London. Series B, Biological sciences},
volume = {381},
number = {1950},
pages = {},
doi = {10.1098/rstb.2025.0045},
pmid = {42132035},
issn = {1471-2970},
support = {//UK Research and Innovation/ ; },
mesh = {Humans ; Indonesia ; Infant ; *Diet ; Case-Control Studies ; *Gastrointestinal Microbiome ; Male ; Female ; RNA, Ribosomal, 16S/analysis ; *Bacteria/classification/isolation & purification/genetics ; },
abstract = {Previous studies have compared the microbiota profiles of stunted and non-stunted children. However, how these profiles interact with dietary patterns is not completely understood. To assess differences in microbial diversity, composition and bacteria taxa between stunted and non-stunted children and how the consumption of food groups influence the gut microbiota of stunted children, this matched case-control study was conducted among 150 pairs of stunted and non-stunted children of between 18-23 months old in East Lombok, Indonesia. Anthropometry and dietary data were collected by trained enumerators. Microbiome data were generated by sequencing the V4 hypervariable region of the 16S rRNA gene. No between-group differences in alpha and beta diversity were observed. Exploratory analysis identified that Agathobacter, Coprococcus, Dorea, Hominimerdicola, Lawsonibacter and Ruminococcoides were more proportionally abundant among non-stunted children and Peptostreptococcus among stunted children. However, there was no association between food group consumption and abundance of these taxa. Breastfeeding significantly shaped the microbiota profiles. Future research on the association between microbiota profiles and complementary feeding should incorporate approaches such as diet modelling to capture the combined contributions of food groups and dietary components, alongside longitudinal study designs. This article is part of the theme issue 'Biological, biomedical and environmental drivers of stunting'.},
}

Humans
Indonesia
Infant
*Diet
Case-Control Studies
*Gastrointestinal Microbiome
Male
Female
RNA, Ribosomal, 16S/analysis
*Bacteria/classification/isolation & purification/genetics

@article {pmid42132238,
year = {2026},
author = {Roostaei, G and Riahi, T and Nikfar, S and Abdollahi, M},
title = {Harnessing the immune system in lung cancer: emerging role of the microbiome.},
journal = {Expert review of clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1080/1744666X.2026.2661805},
pmid = {42132238},
issn = {1744-8409},
abstract = {INTRODUCTION: The microbiome has emerged as a critical regulator of tumor biology and immune response in lung cancer. Once considered sterile, the lung is now recognized to harbor a diverse microbiome that interacts with the gut - lung axis to shape inflammation, immune evasion, and therapeutic outcomes.

AREAS COVERED: This study reviews current evidence linking microbiome composition and function to lung cancer development and response to immune checkpoint inhibitors (ICIs). We explore mechanisms of microbial influence on host immunity, identify key taxa associated with treatment outcomes, and summarize therapeutic strategies such as fecal microbiota transplantation, probiotics, postbiotics, dietary changes, antibiotics, and engineered live biotherapeutics. The literature search was performed across multiple databases and sources, including PubMed, Scopus, Embase, and clinical trial registries, up to August 2025, focusing on both preclinical and clinical studies related to lung cancer, immunotherapy, and microbiome-targeted interventions.

EXPERT OPINION: Microbiome research is redefining precision oncology by presenting new biomarkers and therapeutic targets. Although early-phase trials show potential to improve ICI efficacy, implementation is limited by donor variability, methodological differences, and biosafety issues. Standardized protocols, mechanistic studies, and biomarker-driven patient selection will be crucial to incorporating microbiome modulation into routine lung cancer treatment.},
}

@article {pmid42132389,
year = {2026},
author = {Hickey, E and Pradhan, A and Ma, Q and Leaves, I and Philip-Brookes, A and Duggan, S and Harvey, JA and Dambuza, IM and Cherek, P and Yuecel, R and d'Enfert, C and Gow, NAR and Brown, GD and Brown, AJP},
title = {The prebiotic inulin affects virulence factor expression in Candida albicans.},
journal = {mBio},
volume = {},
number = {},
pages = {e0385125},
doi = {10.1128/mbio.03851-25},
pmid = {42132389},
issn = {2150-7511},
abstract = {Dietary supplementation with prebiotics such as inulin has been associated with a broad range of health benefits. However, the effects of inulin on the opportunistic fungal pathogen Candida albicans, which resides as a commensal in the gut, have not been characterized. Here, RNA sequencing revealed that inulin affects the expression of C. albicans genes associated with cell wall construction, adhesion, and yeast-hypha morphogenesis. Consistent with these changes in gene expression, inulin inhibited hyphal development, increased adhesion to human Caco-2 and A431 cells, decreased the thickness of the inner layer of the C. albicans cell wall, reduced the exposure of cell wall pathogen-associated molecular patterns [β-(1,3)-glucan and chitin], and affected antifungal drug sensitivity. These changes impacted host immune recognition and cytokine responses, ultimately attenuating the virulence of C. albicans in an invertebrate infection model. Therefore, dietary supplementation with inulin is likely to influence host-fungus interactions.IMPORTANCEThe benefits of prebiotic dietary supplements, such as inulin (a natural plant dietary fiber), are thought to include a healthier gut microbiome, a reduced risk of colon cancer, and lower cholesterol levels. Unsurprisingly, prebiotic usage is increasing rapidly. However, while the effects of prebiotics upon gut bacteria have been characterized, the impacts upon Candida albicans, an opportunistic fungal pathogen that resides in the human gut, have remained obscure. We show that inulin affects the expression of virulence-related phenotypes and antifungal drug sensitivity in Candida. Furthermore, we show that inulin reduces the virulence of this fungus in an invertebrate model, consistent with the idea that inulin may lower the risk of fungal infection in healthy individuals.},
}

@article {pmid42132693,
year = {2026},
author = {Martínez-Subirá, M and Cortijo Alfonso, ME and Friero, I and Macià, A and Pena, RN and Molinero, N and Moreno-Arribas, MV and Rubió-Piqué, L and Moralejo, M},
title = {Barley extrudates modulate the gut microbiome-metabolome axis in vitro through β-glucan fermentation and polyphenol biotransformation.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d6fo00601a},
pmid = {42132693},
issn = {2042-650X},
abstract = {Barley is rich in fermentable dietary fiber and phenolic compounds, both of which have recognized benefits for gut health and whose functionality is influenced by processing. Here, four barley genotypes differing in β-glucan content, type of starch, and phenolic profiles were extruded to obtain ready-to-eat products, which were then evaluated using a combined in vitro digestion-colonic fermentation model. The gastrointestinal fate of β-glucans and phenolics, short-chain fatty acids production, phenolic metabolite formation, and gut microbiota composition were assessed. After digestion, substantial amounts of β-glucans and phenolics remained in the non-bioaccessible fraction, supporting their relevance as substrates for colonic fermentation. During fermentation, the β-glucan-rich genotypes Annapurna® and Hilose® showed the strongest butyrogenic response, while the purple-grain genotype DHL-151340, characterized by a flavone- and anthocyanin-rich profile, showed an earlier and more pronounced accumulation of low-molecular-weight phenolic catabolites. Compared with the control, barley extrudates induced time-dependent shifts in microbiota composition, although community profiles tended to converge at later fermentation stages. Overall, genotype- and processing-driven differences translated into distinct fermentation and phenolic biotransformation footprints, highlighting the relevance of barley matrix composition in shaping the colonic fate of cereal bioactive compounds.},
}

@article {pmid42132952,
year = {2026},
author = {Özel, Ş and Lauritano, D},
title = {Oral mucosal microbiome alterations in recurrent aphthous stomatitis: a systematic review of 16 S rRNA gene sequencing studies.},
journal = {Molecular biology reports},
volume = {53},
number = {1},
pages = {},
pmid = {42132952},
issn = {1573-4978},
mesh = {Humans ; *Stomatitis, Aphthous/microbiology/genetics ; *Mouth Mucosa/microbiology ; *RNA, Ribosomal, 16S/genetics ; *Microbiota/genetics ; Dysbiosis/microbiology ; Case-Control Studies ; Saliva/microbiology ; Bacteria/genetics/classification ; Recurrence ; },
abstract = {Recurrent aphthous stomatitis (RAS) is a prevalent inflammatory disorder of the oral mucosa characterized by recurrent painful ulcerations in otherwise healthy individuals. This systematic review aimed to evaluate alterations in the oral mucosal microbiome of patients with RAS based on studies using 16 S rRNA sequencing. A systematic search of PubMed, Scopus, and Web of Science was conducted on April 14, 2026. Eligible studies included human case-control investigations evaluating oral mucosal swab samples from patients with clinically diagnosed RAS and healthy controls using 16 S rRNA sequencing. Studies based solely on saliva, culture methods, PCR-only analyses, or lacking controls were excluded. Joanna Briggs Institute Critical Appraisal Checklist for Case-Control Studies was used for the evaluation of selected articles. Six studies met the inclusion criteria. Considerable heterogeneity was observed in alpha and beta diversity outcomes. Most studies reported reduced microbial richness in RAS lesions, whereas others found increased or unchanged diversity. Ulcerated sites frequently demonstrated reduced abundance of health-associated taxa such as Streptococcus and Firmicutes, with increased levels of Proteobacteria and inflammation-associated genera including Neisseria, Haemophilus, Prevotella, and Fusobacterium. Microbial alterations were most pronounced at active ulcer sites, while non-ulcerated or healed mucosa more closely resembled healthy controls. Current evidence suggests that RAS is associated with localized, site-specific microbial dysbiosis rather than generalized oral microbiome disruption. However, methodological heterogeneity and small sample sizes limit definitive conclusions. Future standardized longitudinal studies integrating functional metagenomics are warranted to clarify the role of the microbiome in RAS pathogenesis.},
}

Humans
*Stomatitis, Aphthous/microbiology/genetics
*Mouth Mucosa/microbiology
*RNA, Ribosomal, 16S/genetics
*Microbiota/genetics
Dysbiosis/microbiology
Case-Control Studies
Saliva/microbiology
Bacteria/genetics/classification
Recurrence

@article {pmid42132964,
year = {2026},
author = {He, P and Stein, E},
title = {The Microbiome and Esophageal Disease: Where Are We Now?.},
journal = {Current gastroenterology reports},
volume = {28},
number = {1},
pages = {},
pmid = {42132964},
issn = {1534-312X},
mesh = {Humans ; *Esophageal Diseases/microbiology ; *Microbiota ; Gastroesophageal Reflux/microbiology ; Barrett Esophagus/microbiology ; *Esophagus/microbiology ; Dysbiosis/microbiology ; Eosinophilic Esophagitis/microbiology ; *Gastrointestinal Microbiome ; },
abstract = {PURPOSE OF REVIEW: The microbiome in the esophagus has been an area of early active investigation. In the past 5 years, advancements in next-generation sequencing and computational analysis have provided a more detailed picture of the esophageal microbiome. This review will examine the most recent advances in the past 5 years on the study of microbiome changes in healthy and diseased esophagus to better understand the link between microbiome and esophageal diseases, potentially leading to new prevention or treatment strategies.

RECENT FINDINGS: The microbiome has a key set of baseline parameters in the usual or non-diseased esophageal lumen. There are measurable changes in the baseline microbiome species of different disease phenotypes including eosinophilic esophagitis, gastroesophageal reflux disease, Barrett's esophagus and achalasia. Some studies suggest that certain microbiome features may even be associated with worse outcomes. Dysbiosis of esophageal microbiome is implicated in various esophageal disorders, including GERD, Barrett's esophagus, EoE, and achalasia. However, confounding factors such as antibiotic use, PPI use, dietary habits, and geographic location influence microbiome variability and make the standardized study of this field challenging. The next phase of research will need to include more focus on larger scale studies with reproducible parameters. As some features of the microbiome are associated with disease progression, there are multiple new avenues of intervention potentially available with an improved understanding of the human esophageal microbiome.},
}

Humans
*Esophageal Diseases/microbiology
*Microbiota
Gastroesophageal Reflux/microbiology
Barrett Esophagus/microbiology
*Esophagus/microbiology
Dysbiosis/microbiology
Eosinophilic Esophagitis/microbiology
*Gastrointestinal Microbiome

@article {pmid42132991,
year = {2026},
author = {He, WT and Xing, X and Wang, F and Li, L and Cheng, Y and Yao, G},
title = {Innovative technologies and future perspectives in tumor microbiomics.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {42132991},
issn = {1869-1889},
abstract = {Microorganisms within the tumor microenvironment represent an important but still underexplored dimension of cancer biology, influencing genomic stability, immune responses, metabolism, and therapeutic efficacy. Although recent findings underscore the significance of the tumor microbiome, distinguishing causal "drivers" from non-functional "passengers" remains a major challenge, particularly in the context of extremely low microbial biomass and high contamination risk. Advances in next-generation sequencing, single-cell genomics, and spatial transcriptomics are now transforming the field, enabling profiling that extends beyond descriptive catalogs toward functional and spatial resolution. Here, we introduce a unified, contamination-aware analytical framework tailored to the unique constraints of tumor microbiome studies, integrating standardized sampling, library construction, host-depletion strategies, and multi-layer computational analysis. We also evaluate emerging technologies that couple microbial identity with host-cell states at single-cell and spatial resolution, offering new opportunities to functionally map tumor-associated microorganisms. Furthermore, we propose that the integration of orthogonal validation strategies-combining imaging, spatial transcriptomics, in situ microbial profiling, and sequencing-is poised to define the next stage of mechanistic tumor microbiome research. Together, these perspectives outline key methodological inflection points and future directions toward a mechanistic understanding of tumor-microbe interactions and their therapeutic potential.},
}

@article {pmid42133003,
year = {2026},
author = {Munir, A and Tarannum, T and Saad, N and Abdaal, M},
title = {Effectiveness of Non-Antibiotic Therapies in the Management of Recurrent Urinary Tract Infections in Women: A Systematic Review.},
journal = {International urogynecology journal},
volume = {},
number = {},
pages = {},
pmid = {42133003},
issn = {1433-3023},
abstract = {INTRODUCTION AND HYPOTHESIS: Recurrent urinary tract infections (rUTIs) are a prevalent condition in women, historically managed with continuous low-dose antibiotic prophylaxis. However, the global rise in antimicrobial resistance (AMR) necessitates the evaluation of non-antibiotic alternatives. This study was aimed at evaluating the efficacy and safety of non-antibiotic therapies, specifically D-mannose, cranberry products, probiotics, topical estrogen, methenamine hippurate, and immunoprophylaxis in preventing rUTIs in adult women.

METHODS: A systematic review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines. We searched PubMed, Europe PMC, Science Direct, and the Cochrane Library for randomized controlled trials (RCTs) and high-quality observational studies published up to 31 January 2025. Studies were assessed for risk of bias using the Cochrane RoB 2 tool and the Newcastle-Ottawa Scale. The primary outcome was the reduction in UTI recurrence rates.

RESULTS: Twelve studies met the inclusion criteria (10 RCTs, 2 observational studies). Methenamine hippurate was found to be non-inferior to daily antibiotic prophylaxis in preventing rUTIs. Immunoprophylaxis with the sublingual vaccine MV140 significantly reduced recurrence compared with placebo, with 56-58% of women remaining UTI free in a large RCT. Vaginal estrogen proved effective for postmenopausal women, significantly reducing recurrence, despite small sample sizes in recent trials. D-mannose demonstrated efficacy equivalent to antibiotics in specialist settings, but showed no benefit over placebo in a broad primary care population. Cranberry products were generally less effective than antibiotics but prevented the development of resistant fecal flora. Probiotics significantly prolonged the time to first recurrence.

CONCLUSIONS: Non-antibiotic therapies offer viable, safe, and effective alternatives to long-term antibiotics. The evidence supports a stratified approach: methenamine hippurate and vaginal estrogen (in postmenopausal women) are supported by level 1 evidence as first-line non-antibiotic alternatives. MV140 immunoprophylaxis demonstrates high efficacy in recurrent phenotypes. D-mannose and cranberry show mixed efficacy and should be reserved for selected patient populations, particularly in specialist settings.},
}

@article {pmid42133231,
year = {2026},
author = {Yiu, CH and Winardi, K and Lu, CY},
title = {Immunological Drug-Drug Interactions in Immune Checkpoint Inhibitor Therapy: Mechanisms, Clinical Evidence, and Artificial Intelligence.},
journal = {Current oncology reports},
volume = {28},
number = {1},
pages = {},
pmid = {42133231},
issn = {1534-6269},
mesh = {Humans ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology/adverse effects ; Drug Interactions ; *Artificial Intelligence ; *Neoplasms/drug therapy/immunology ; Gastrointestinal Microbiome/drug effects ; Tumor Microenvironment/drug effects/immunology ; },
abstract = {PURPOSE OF REVIEW: Immune checkpoint inhibitors (ICIs) have transformed cancer therapy, producing durable responses across multiple malignancies. However, treatment outcomes may be influenced by immunological drug-drug interactions (DDIs) arising from commonly prescribed concomitant medications. Unlike classical pharmacokinetic or pharmacodynamic DDIs, these interactions operate through systemic mechanisms that modulate anti-tumour immunity, including alterations to the gut microbiome, immune signalling pathways, and the tumour microenvironment. This review proposes a conceptual framework for "immunological DDIs" (iDDIs), extending beyond metabolic interactions toward a system-level understanding of immune regulation.

RECENT FINDINGS: We synthesise current evidence on commonly used medication classes-organised by their primary immunological mechanisms: (1) gut microbiome-mediated effects, (2) systemic immunosuppression, and (3) tumour microenvironment modulation-and their impact on ICI efficacy and safety. Meta-analyses suggest that certain medications, particularly antibiotics and proton pump inhibitors, are associated with poorer clinical outcomes, although confounding by indication and disease severity remain important limitations. Artificial intelligence (AI) is an emerging approach to detect and characterise complex DDIs using large-scale clinical and real-world data. Natural language processing, machine learning models, and large language models show potential for extracting medication exposure, predicting adverse events, and supporting clinical decision-making. Most AI applications remain at an early stage, with limited external validation and uncertain clinical utility. Future research should integrate mechanistic biology, prospective clinical studies, and explainable AI approaches to improve identification of iDDIs and optimise the safe and effective use of ICIs in oncology.},
}

Humans
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology/adverse effects
Drug Interactions
*Artificial Intelligence
*Neoplasms/drug therapy/immunology
Gastrointestinal Microbiome/drug effects
Tumor Microenvironment/drug effects/immunology

@article {pmid42133449,
year = {2026},
author = {Skrabulyte-Barbulescu, J and Yassin, LK and Almazrouei, S and Alkuwaiti, SH and Almarzooqi, S and Alnuaimi, F and Alketbi, S and Nakhal, MM and Rutkowska-Gauvry, P and Matar, SA and Hamad, MIK},
title = {Parental microbiome programming of early-life neurodevelopment: multi-niche contributions through the microbiome-gut-brain axis.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2673888},
doi = {10.1080/19490976.2026.2673888},
pmid = {42133449},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Female ; *Brain/growth & development ; Pregnancy ; Male ; Infant ; *Brain-Gut Axis ; Animals ; Child Development ; },
abstract = {The microbiota-gut-brain axis (MGBA) is a central pathway through which gut microbial communities influence neurodevelopment via immune, metabolic, and neural signalling. Early life, spanning preconception through infancy, represents a particularly sensitive window during which parental microbiomes exert disproportionate influence on offspring gut colonization, immune education, and neurodevelopmental programming. This review synthesizes current evidence on how maternal and paternal microbiomes shape pediatric neurodevelopment through coordinated microbial, metabolic, immune, and epigenetic pathways. We examine pregnancy-associated remodeling of maternal microbiomes across gut, vaginal, oral, skin, and milk niches, highlighting how hormonal, metabolic, and immune adaptations drive site-specific microbial shifts with downstream consequences for fetal and infant brain development. Core microbial mechanisms are discussed, including short-chain fatty acids (SCFAs), tryptophan-derived metabolites, bile-acid signaling, and immune mediators that link microbial metabolism with immune and neurodevelopmental processes. These mechanisms are integrated with key transmission routes, including placental metabolite transfer, mode-of-delivery-dependent microbial seeding, breast milk-mediated signaling, and early environmental exposures that further shape the developing MGBA. We also incorporate emerging evidence on paternal microbiome contributions via preconception programming, sperm epigenetic remodeling, and germline-microbiome interactions, expanding the traditional maternal-centric view of intergenerational microbial inheritance. Finally, we evaluate modifiable factors, including diet, metabolic status, stress, antibiotic exposure, and microbiome-targeted interventions, and discuss their translational relevance. While associations between the microbiome and neurodevelopment are increasingly supported by human studies, many mechanistic insights remain derived from animal models, and causal relationships are not yet fully established. By integrating mechanistic, clinical, and systems-level perspectives, this review positions the MGBA as a promising but still evolving framework for understanding and potentially modulating early-life brain development.},
}

Humans
*Gastrointestinal Microbiome/physiology
Female
*Brain/growth & development
Pregnancy
Male
Infant
*Brain-Gut Axis
Animals
Child Development

@article {pmid42133532,
year = {2026},
author = {Bravo Iniguez, A and Sun, Q and Du, M and Zhu, MJ},
title = {Unearthing the bioactive properties of potato (Solanum tuberosum) for improving metabolic health.},
journal = {Critical reviews in food science and nutrition},
volume = {},
number = {},
pages = {1-20},
doi = {10.1080/10408398.2026.2662981},
pmid = {42133532},
issn = {1549-7852},
abstract = {Worldwide, both adults and children continue to develop metabolic diseases at an alarming rate. Metabolic syndrome (MetS) refers to a cluster of risk factors associated with an increased risk of noncommunicable diseases. The development of MetS is complex, and its mitigation requires multiple complementary strategies. One promising approach is dietary intervention with nutraceutical-rich foods that strengthen metabolic organs such as the liver and intestines against oxidative stress and inflammation. Potatoes are a widely consumed crop grown globally and are rich in macronutrients and bioactive secondary metabolites, including phenolic acids, carotenoids, and anthocyanins. They also provide resistant starch and dietary fiber that reach the colon undigested, where they positively modulate the gut microbiome, enhance short-chain fatty acid production, and reinforce the intestinal epithelial barrier. This review summarizes how different potato varieties and their chemical constituents mitigate hallmarks of MetS through both direct and indirect mechanisms. Additionally, it discusses molecular pathways induced by potato polyphenols and microbial metabolites that may underlie these effects, with particular emphasis on mediators linking metabolism to intestinal epithelial homeostasis. Current limitations and knowledge gaps are also highlighted, emphasizing the need for standardized potato-based interventions and expanded evaluation of skeletal muscle outcomes.},
}

@article {pmid42133581,
year = {2026},
author = {Herrington, RTB and Lyu, Z and Raman, R and Seda, SE and Snyder, C and Bivens, NJ and Lei, Z and Islam, T and Sumner, LW and Joshi, T and Rosenfeld, CS},
title = {Disturbances of the Placenta-Brain Axis in Germ-Free Pregnant Mice.},
journal = {Biology of reproduction},
volume = {},
number = {},
pages = {},
doi = {10.1093/biolre/ioag103},
pmid = {42133581},
issn = {1529-7268},
abstract = {Maternal gut microbiota changes can profoundly shape on offspring health. The placenta may be vulnerable to maternal gut microbiota alterations. Placental disruptions can influence fetal brain development and underly risks for neurobehavioral disorders. Maternal gut microbiota disruptions might affect the placenta through alterations in bacterial short chain fatty acids (SCFA). The hypothesis tested is that depletion of maternal gut microbiota, as may occur in pregnant women treated with antibiotics and germ-free (GF) mice, impacts bacterial SCFA in her fecal samples and in placenta and fetal brain. We assessed whether transcriptomic changes would be evident in placenta and fetal brain from conceptuses derived from GF relative to multi-pathogen free (MPF) pregnant females. Maternal GF status reduced the concentrations of all measured SCFA within the stool. Surprisingly, two-methylbutanoic acid was significantly increased in male and female placenta and fetal brain samples in conceptuses from GF dams. In female and male placenta, several Prl form had altered expression in conceptuses from GF dams. In male placenta from GF dams, Hsd11b2 and Dio3 showed increased expression. Decreased expression of Sl6a2 and Slc22a3 in female fetal brain from GF dams might influence uptake of catecholamines. Results reveal depletion of maternal microbiota can lead to striking effects on the placenta-fetal brain axis. Findings raise concern as to whether maternal microbiota alterations due to other intrinsic or extrinsic factors, namely antibiotic treatment, might impact transcriptomic profiles in fetal placenta and brain. Underlying mechanisms remain uncertain but may relate to changes bacterial metabolites transferred from mother to conceptus.},
}

@article {pmid42134120,
year = {2026},
author = {Liang, W and Nong, Q and Huang, H and Huang, J and Shao, J and Wang, M and Hong, P and Liu, S and Zhou, C and Zhong, S},
title = {Correlation analysis between microbial diversity in mixed-fermented shrimp juice and the synthesis pathways of characteristic flavor compounds.},
journal = {Food chemistry},
volume = {518},
number = {},
pages = {149574},
doi = {10.1016/j.foodchem.2026.149574},
pmid = {42134120},
issn = {1873-7072},
abstract = {This study elucidated flavor formation in fermented shrimp juice using metagenomics and correlation analyses. The amino acid nitrogen content peaked at 0.54 g/100 mL on the 30th day, surpassing that of traditional fish sauce. Phenolic compounds, including guaiacol and phenylacetaldehyde, were identified as key flavor contributors. The microbial community gradually developed into a stable microbiota dominated by nine genera, including Aspergillus, Lactiplantibacillus, and Meyerozyma. Metagenomic analysis demonstrated that this core microbiome governed critical metabolic pathways for carbohydrate, amino acid, and lipid metabolisms, collectively driving the efficient flavor development in the fermented product.},
}

@article {pmid42134193,
year = {2026},
author = {Mao, C and Chen, D and Lai, Y and Lu, M and Wang, C},
title = {MMP1 Modulates Head and Neck Squamous Cell Carcinoma Progression and Therapeutic Response Via Tumour Microenvironment.},
journal = {International dental journal},
volume = {76},
number = {4},
pages = {109621},
doi = {10.1016/j.identj.2026.109621},
pmid = {42134193},
issn = {1875-595X},
abstract = {AIM: Head and neck squamous cell carcinoma (HNSCC) is a highly invasive malignancy driven by complex molecular interactions within the tumour microenvironment (TME). This study aimed to investigate the critical role of MMP1 in HNSCC progression, particularly its interplay with the microbiome and immune remodelling, to uncover potential therapeutic targets.

METHODS: We conducted transcriptomic analysis of HNSCC tissues and performed functional experiments in Cal-27 cells using a zebrafish tumour model, including MMP1 knockdown. The effects of TPF chemotherapy, Bifidobacterium longum, and their combination were evaluated in vitro. Additionally, we assessed macrophage recruitment, proinflammatory cytokine expression (IL-6, IL-1B, TNF-A), angiogenesis-related genes (VEGFA), zebrafish transcriptomic profiles, and gut microbiota diversity.

RESULTS: Transcriptomic profiling revealed significant gene expression differences between cancer and healthy tissues, with enrichment in metabolic, neurodegenerative, and cardiovascular pathways. MMP1 was markedly up-regulated in tumours and strongly correlated with invasion and metastasis. Functional studies demonstrated that MMP1 knockdown reduced the efficacy of TPF, B. longum, and their combination, impairing tumour growth suppression, macrophage recruitment, and proinflammatory cytokine expression. However, B. longum partially counteracted MMP1-mediated immune activation, suggesting microbial-immune crosstalk. MMP1 knockdown also retained partial inhibition of angiogenesis-related genes (eg, VEGFA), indicating a selective role in vascular remodelling. Furthermore, MMP1 knockdown attenuated the Cal-27 cell-induced reduction in zebrafish gut microbiome diversity and alterations in transcriptomic expression patterns.

CONCLUSION: Our findings establish MMP1 as a key regulator of HNSCC progression and therapeutic response, influencing microbiome-mediated immune remodelling, inflammation, and angiogenesis. These insights suggest that targeting MMP1 and modulating the microbiome could enhance therapeutic strategies for HNSCC by reshaping the TME. This study provides a foundation for further exploration of TME-targeted interventions in HNSCC treatment.},
}

@article {pmid42134220,
year = {2026},
author = {Li, D and Li, Y and Chi, Y and Hou, Y and Wang, X and Pan, B},
title = {Salinization reduces microbial diversity and drives DOM-mediated community assembly along a river-lake continuum in arid Northwest China.},
journal = {Journal of environmental management},
volume = {408},
number = {},
pages = {129913},
doi = {10.1016/j.jenvman.2026.129913},
pmid = {42134220},
issn = {1095-8630},
abstract = {Hongjiannao Lake, once the largest desert freshwater lake in the arid and semi-arid regions of China, has undergone progressive salinization and ecological degradation over recent decades. During salinization, the cascade effect formed by the molecular transformation of dissolved organic matter (DOM) and the succession of microbial communities has emerged as a key mechanism for unraveling the internal processes of ecosystem degradation. In this study, we integrated hydrochemical parameters, DOM properties, and high-throughput sequencing of 16S rRNA genes to investigate microbiota differentiation and its environmental drivers along the river-lake continuum of the Hongjiannao watershed. The results showed that salinization drove molecular reconstruction of DOM, with a 37.6% decrease in humic-like components and an 84.7% increase in protein-like components. Increases in spectral slope ratio (SR) and specific UV absorbance at 254 nm (SUVA254) further indicated the breakdown of terrestrial humic substances into smaller aromatic molecules. Concurrently, the microbial community exhibited significantly suppressed alpha diversity and reduced spatial heterogeneity; the abundance of ubiquitous freshwater taxa declined, whereas salt-tolerant bacteria (e.g., certain members of Actinomycetota and Cyanobacteriota) increased. Furthermore, the number of functional annotation categories decreased, and the complexity and stability of the microbial co-occurrence network dropped sharply. Salinization drives microbial community reassembly through both direct pathways and indirect effects mediated by DOM transformation. This study reveals a cascading mechanism whereby salinization stress alters DOM bioavailability, leading to a loss of microbial diversity and functional narrowing, ultimately degrading lake ecological functions. We propose an integrated restoration strategy, including ecological water replenishment, introduction of salt-tolerant microbial consortia, and regulation of DOM inputs. This study provides a systematic, microbiome-based framework for the ecological management and restoration of salinized lakes in arid regions.},
}

@article {pmid42134306,
year = {2026},
author = {Barapour, N and Cao, JZ and Wu, Y and Gupta, S and Hoopmann, MR and Qin, R and Midha, MK and Mireault, M and Juanes-Velasco, P and Hanson, C and Ahadi, S and Higgs, E and Baxter, DH and Diener, C and Dagan-Rosenfeld, O and Hornburg, D and Che, S and Edfors, F and Church, SJ and Babu, M and Thota, D and Jin, C and Chou, T and Rego, S and Avina, M and McGuire, L and Li, JW and Karathanos, T and Panyard, DJ and Acosta Parra, MA and Roberts, AK and Ranjit, AK and Rangan, E and Almagro Armenteros, JJ and Ashland, M and Castillo, KE and Traber, G and Ellenberger, M and Kellogg, R and Zhou, W and Rost, H and Kjellberg, M and Mishra, T and Kapil, C and Kusebauch, U and Patwardhan, S and Landeira-Viñuela, A and Hernandez, AP and Thomsen, ME and Mashkoor, M and Sutantiwanichkul, T and Dodig-Crnkovic, T and Bendes, A and Dahl, L and Gibbons, SM and Rangan, PV and Stensballe, A and Schwenk, JM and Unwin, RD and Fuentes, M and Sleno, L and Moritz, RL and Mahal, LK and Snyder, MP},
title = {A comparison of deep multiomics profiles across ethnicity, geography, and age.},
journal = {Cell},
volume = {189},
number = {10},
pages = {3004-3024.e35},
doi = {10.1016/j.cell.2026.04.032},
pmid = {42134306},
issn = {1097-4172},
mesh = {Humans ; Male ; *Ethnicity/genetics ; Female ; Middle Aged ; Adult ; Aged ; Geography ; Microbiota ; *Aging/genetics ; White People/genetics ; Transcriptome ; Metabolomics ; Proteomics ; Genomics/methods ; Diet ; Asian People/genetics ; Multiomics ; White ; },
abstract = {Despite extensive research, molecular differences in human populations and the influence of ancestry, age, geography, and diet are poorly understood. We performed comprehensive multiomics profiling (including genomics, transcriptomics, proteomics, metabolomics, lipidomics, metallomics, glycomics, and microbiomics) on samples from 322 healthy individuals of European, East Asian, and South Asian ancestry across multiple continents. We identified ethnicity-associated molecular features linked to host metabolism, autoimmune disease risk, drug metabolism, and neurodegenerative pathways. We uncovered ancestry- and geography-related molecular changes affecting metabolism, immune function, microbiome composition, and biological aging. Specific genetic variants and gene expression differences were associated with lipid metabolism and immune regulation. Geography influenced biological age: East Asians showed lower biological age in their ancestral regions, whereas individuals of European ancestry exhibited lower biological age in the US/Canada than in Europe. Diet-microbiome metabolism interactions displayed ethnicity-specific patterns, many related to health. This open access resource advances understanding of ethnicity-environment interactions and supports precision medicine.},
}

Humans
Male
*Ethnicity/genetics
Female
Middle Aged
Adult
Aged
Geography
Microbiota
*Aging/genetics
White People/genetics
Transcriptome
Metabolomics
Proteomics
Genomics/methods
Diet
Asian People/genetics
Multiomics
White

@article {pmid42134451,
year = {2026},
author = {Vishwakarma, M and Anitha, K and Ashique, S and Mishra, N},
title = {Advances in siRNA and synbiotic therapies for colorectal cancer: a molecular and microbiota perspective.},
journal = {Drug discovery today},
volume = {},
number = {},
pages = {104697},
doi = {10.1016/j.drudis.2026.104697},
pmid = {42134451},
issn = {1878-5832},
abstract = {Colorectal cancer (CRC) remains a major global health challenge, with rising incidence and mortality despite advances in conventional therapies, often limited by recurrence, toxicity and drug resistance. siRNA-based therapeutics offer a precision approach by selectively silencing oncogenic and chemoresistance-related genes; but their clinical application is hindered by delivery, stability and off-target effects. Concurrently, synbiotics (prebiotics and probiotics) modulate gut microbiota, immune responses and inflammatory pathways involved in CRC progression. Integrating siRNA targeting with synbiotic-mediated microbiome modulation provides a complementary strategy addressing molecular and microenvironmental drivers of CRC. This review highlights key pathways, delivery strategies, co-therapeutic approaches and translational challenges, emphasizing the potential of combined RNAi and microbiome-based therapies for improved CRC management.},
}

@article {pmid42134452,
year = {2026},
author = {Sharma, AK and Akhtar, MS and Orayj, K and Farooqui, S and Khan, A and Sharma, G},
title = {Microbial dysbiosis in metabolic disorders: linking epigenomic regulation and pathological mechanisms.},
journal = {Drug discovery today},
volume = {},
number = {},
pages = {104698},
doi = {10.1016/j.drudis.2026.104698},
pmid = {42134452},
issn = {1878-5832},
abstract = {Microbial dysbiosis critically contributes to metabolic disorders by altering host-microbiome interactions and disrupting metabolic homeostasis. This review highlights how dysbiosis-derived metabolites, including short-chain fatty acids (SCFA) and trimethylamine-N-oxide (TMAO), modulate epigenetic mechanisms such as DNA methylation, histone modification, and non-coding RNA expression in key metabolic tissues. These epigenomic changes impair insulin signaling, lipid metabolism, and inflammatory responses. We further explore the potential of microbial-epigenetic biomarkers for early diagnosis of metabolic disease. Moreover, we assess emerging microbiome-based therapies including prebiotics, SCFA supplementation, and fecal microbiota transplantation for their ability to reverse epigenetic dysregulation. Understanding the microbiome-epigenome-metabolism axis may enable precision diagnostics and targeted interventions for obesity, type 2 diabetes, and related disorders.},
}

@article {pmid42134481,
year = {2026},
author = {Aburahma, A and Canfield, JR and Sprague, JE and Fernandez, AM},
title = {Gut Microbiome Modulation of Opioid Reinforcement in Preclinical Models: Microbial Regulation of Reward and Motivation.},
journal = {Brain research bulletin},
volume = {},
number = {},
pages = {111938},
doi = {10.1016/j.brainresbull.2026.111938},
pmid = {42134481},
issn = {1873-2747},
abstract = {Emerging evidence indicates that the gut microbiome modulates opioid-related behaviors through bidirectional communication with mesolimbic reward circuitry. Preclinical studies show that antibiotic-induced microbiome depletion, germ-free conditions, and developmental microbial disruption alter opioid reward and reinforcement in animal models. Rather than uniformly increasing or decreasing opioid responsivity, microbiome disruption produces paradigm-specific and stage-dependent effects across distinct components of reinforcement learning. Reduced microbial diversity is associated with decreased production of short-chain fatty acids (SCFAs), altered gut barrier integrity, and enhanced peripheral immune signaling. These changes converge on the ventral tegmental area (VTA) and nucleus accumbens (NAc), modifying dopaminergic transmission and transcriptional plasticity within reward-related circuits. Notably, microbiome depletion reduces morphine conditioned place preference, whereas, in separate paradigms, it increases fentanyl self-administration and motivational responding under progressive ratio schedules, revealing a dissociation between hedonic reward and reinforcement processes. SCFA supplementation can partially rescue reward-related phenotypes, supporting a mechanistic role for microbial metabolites. Across reinforcement paradigms, microbiome status emerges as a dynamic regulator of opioid reinforcement rather than a simple modulator of reward magnitude. Importantly, antibiotic exposure, which is common during infectious disease treatment of individuals with opioid use disorder (OUD), may represent a clinically relevant and underappreciated modifier of reinforcement sensitivity and relapse risk. This review uniquely integrates microbiome disruption, stress sensitivity, negative affect, and neuroimmune priming during protracted abstinence to highlight antibiotic exposure as an overlooked but actionable factor in OUD recovery.},
}

@article {pmid42134511,
year = {2026},
author = {Kang, MJ and Lee, KR and Kim, MJ and Jeong, HC and Chae, YJ},
title = {Gut microbiome-related tryptophan metabolites modulate drug transporters, with prominent effects on OAT1 and OAT3.},
journal = {Toxicology and applied pharmacology},
volume = {},
number = {},
pages = {117868},
doi = {10.1016/j.taap.2026.117868},
pmid = {42134511},
issn = {1096-0333},
abstract = {The gut microbiome plays a key role in tryptophan metabolism by directly generating indole derivatives and indirectly modulating the host-driven kynurenine pathway via microbial metabolites. In this study, we examined the effects of 12 gut microbiome-related tryptophan metabolites on major drug transporters. In vitro assays using transporter-overexpressing cell lines revealed that indole-3-acrylic acid (IA), indole-3-propionic acid (IPA), kynurenic acid (KA), and xanthurenic acid (XA) inhibited organic anion transporter 1 (OAT1) and organic anion transporter 3 (OAT3) activity by up to 83.7%, with half-maximal inhibitory concentration (IC50) values ranging from 5.41 to 121 μM for OAT1 and 0.31 to 9.50 μM for OAT3. Molecular docking analysis provided qualitative support for potential interactions with OAT1. In vivo pharmacokinetic studies in rats showed that the coadministration of these metabolites significantly increased systemic exposure of furosemide, a representative OAT1/OAT3 substrate, by 1.3- to 2.9-fold and was accompanied by changes in renal excretion. In contrast, most metabolites showed minimal effects on other transporters such as organic anion transporting polypeptide 1B1/1B3 (OATP1B1/OATP1B3), organic cation transporter 2 (OCT2), multidrug and toxin extrusion 1 (MATE1), multidrug resistance protein 1 (MDR1), and breast cancer resistance protein (BCRP). These findings provide mechanistic in vitro evidence that selected gut microbiome-related tryptophan metabolites interact with OAT1/OAT3 and proof-of-concept rat pharmacokinetic data showing altered furosemide disposition after metabolite coadministration. Further studies are required to determine whether these transporter-related effects are clinically relevant in humans.},
}

@article {pmid42134583,
year = {2026},
author = {Berninghaus, AE and Radniecki, TS},
title = {Influence of feedstock and operational parameters on the composition, temporal dynamics, and sensitivity of microbiomes from nineteen full-scale anaerobic municipal sludge digesters and anaerobic fat, oil, and grease co-digesters.},
journal = {Bioresource technology},
volume = {},
number = {},
pages = {134877},
doi = {10.1016/j.biortech.2026.134877},
pmid = {42134583},
issn = {1873-2976},
abstract = {Anaerobic co-digestion is a key microbial-based technology in the bioeconomy. However, the effects of lipidic co-substrates on full-scale anaerobic digester microbiomes, including composition, structure and sensitivity to organic overload shocks, have yet to be fully explored. This study sequenced 12 wastewater solids mono-digesters and 7 high-strength lipidic waste co-digesters monthly for 14 months. The presence of co-substrates enriched hydrolytic bacteria, fermentative bacteria and acetoclastic methanogens, resulting in a novel co-digester core microbiome. It also decreased microbiome richness, alpha diversity, structural fluidity (i.e., mean rank shifts - MRS), and the relative abundance of sub-dominant bacterial taxa (from 45 % to 37 %). The less rich and more compositionally stable microbiomes of anaerobic co-digesters resulted in higher methane yields at lower organic shock loads (i.e., 1 mL of canola oil) compared with anaerobic mono-digesters (239.9 ± 54.6 mL CH4/mL canola oil and 87.5 ± 22.3 mL CH4/mL canola oil, respectively). However, anaerobic co-digesters had greater sensitivity to higher organic shock loads (5-20 mL of canola oil), quantified by percent reduction of methane yields, compared to anaerobic mono-digesters. A multivariate linear regression model predicting a full-scale anaerobic digester's sensitivity to organic overload shocks (Significance F = 1.99 × 10[-12]) revealed that higher operational temperature (p < 0.00) and lower bacterial richness (p < 0.00), archaeal richness (p < 0.00), bacterial MRS (p = 0.02) and archaeal MRS (p < 0.00) increased the sensitivity of anaerobic digesters to organic overloads. Thus, several co-digestion adaptations that contributed to higher methane yields at lower organic shock loads (e.g., lower bacterial richness and greater microbiome compositional stability), also led to greater sensitivity to higher organic shock loads.},
}

@article {pmid41923033,
year = {2026},
author = {Guo, Z and Yu, X and Liu, Y and Hu, Q and Zhang, Z and Zhang, C and Li, J},
title = {A comparative analysis of oral microbial communities in hypertensive patients with and without chronic periodontitis.},
journal = {BMC oral health},
volume = {26},
number = {1},
pages = {},
pmid = {41923033},
issn = {1472-6831},
support = {2025A03J4171//Science and Technology Projects in Guangzhou/ ; },
abstract = {BACKGROUND: Hypertension and chronic periodontitis are both highly prevalent diseases with a well-established association. Dysbiosis of the oral microbiota, a key factor in oral health, may contribute to the mechanisms underlying their comorbidity. This study aimed to characterize the oral microbiota in hypertensive patients with and without periodontitis and explore its potential role in this disease association.

METHODS: Saliva samples from hypertensive patients without periodontitis (T, n = 17), periodontitis patients without hypertension (P, n = 18), comorbid patients (TP, n = 16), and healthy controls (HC, n = 16) underwent 16S rRNA gene (V3-V4) sequencing. Microbiota composition, diversity, differential taxa, and predicted function were analyzed.

RESULTS: Alpha diversity (Chao1/Ace indices) was significantly higher in HC versus disease groups (P < 0.05), while beta diversity showed greater similarity among disease groups but marked divergence from HC (P < 0.05). At genus/species levels, disease groups exhibited characteristic dysbiosis: the abundance of health-associated taxa decreased, while classic periodontal pathogens were significantly enriched. Notably, Streptococcus sp. I-G5 was uniquely enriched in the T group. Functionally, disease groups exhibited enriched lipid metabolism, immune response, and oxidative stress pathways (P < 0.05), contrasting with HC group dominance in xenobiotic biodegradation and amino acid metabolism. Ten differentially abundant genera and eleven species distinguished disease states, highlighting microbiome dysbiosis and metabolic shifts in oral-systemic disease interactions.

CONCLUSION: The oral microbial community of hypertensive patients exhibited dysbiosis analogous to those observed in periodontitis, characterized by a reduced alpha diversity, an enrichment of periodontal pathogens, and activation of pro-inflammatory metabolic pathways. These findings suggest that oral microbial dysbiosis is a shared feature in hypertensive and periodontitis patients. The specific enrichment of Streptococcus sp. I-G5 in hypertension alone may indicate a potential microbial signature for this condition, contributing to a better understanding of the oral microbiome’s role in hypertension.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12903-026-08144-6.},
}

@article {pmid42122957,
year = {2026},
author = {Terry, C and Hall, LA and Halle-Smith, J and Edwards, LA and Sivakumar, S and Chapple, I and Beggs, A and Iqbal, T and Roberts, KJ},
title = {Pancreatic Cancer in the Holobiont and Therapeutic Targets: A Review.},
journal = {Journal of clinical medicine},
volume = {15},
number = {9},
pages = {},
pmid = {42122957},
issn = {2077-0383},
abstract = {Increasing evidence suggests pancreatic cancer develops within a host-microbe ecosystem in which microbial communities across anatomical niches interact with tumour biology, immune regulation, metabolism, and therapeutic response. This review examines pancreatic cancer through the lens of humans as holobionts, integrating evidence from the oral, gut, biliary, and intratumoural microbiomes. Epidemiological and sequencing studies demonstrate consistent microbial alterations across these niches in pancreatic cancer, including oral dysbiosis associated with periodontal pathogens, gut microbial shifts toward pro-inflammatory taxa, disease-specific biliary microbial signatures, and the presence of distinct intratumoural microbial communities. Mechanistic studies indicate that intestinal barrier disruption, microbial translocation, immune and metabolite signalling can influence tumour immune architecture, macrophage polarisation, T-cell infiltration, oncogenic signalling pathways, and chemotherapeutic metabolism, particularly inactivation by tumour-associated bacteria. Microbiome-driven shifts in immunometabolism can reprogramme immune-cell metabolic pathways, impairing effective T-cell activation, promoting tumour-supportive macrophage phenotypes. Emerging therapeutic strategies aim to modulate the microbiome-tumour axis, including dietary interventions, probiotics and immunonutrition, faecal microbiota transplantation, engineered microbial therapies, and microbiome-informed antibiotic strategies. While pre-clinical findings are compelling and early-phase clinical studies suggest feasibility, most evidence remains associative and heterogeneous across cohorts and methodologies. Understanding pancreatic cancer as a multi-site ecological system may help explain inter-patient variability in disease progression and treatment response. This could usher in a new era for therapeutic manipulation where future progress will depend on longitudinal, multi-omic, and interventional studies to determine whether microbiome-targeted strategies can produce clinically meaningful improvements in pancreatic cancer outcomes.},
}

@article {pmid42123280,
year = {2026},
author = {Aljaraedah, T and Al-Thnaibat, S and Nawasreh, AA and Alraei, W and Al-Trad, E},
title = {A Scoping Review of Gut Dysbiosis and Malnutrition in Neurological Disorders: Implications, Indications, and Promising Therapeutic Approaches.},
journal = {Journal of clinical medicine},
volume = {15},
number = {9},
pages = {},
pmid = {42123280},
issn = {2077-0383},
abstract = {Background/Objectives: Neurological diseases are increasing worldwide, but the biological processes underlying these diseases remain poorly understood, and existing treatments have been ineffective at arresting disease progression. Emerging data indicate that dysbiosis of the microbiota-gut-brain axis and malnutrition are comorbid factors in neurological dysfunction. Methods: An extended search strategy was developed using a multifaceted approach across various databases to identify eligible studies published between January 2010 and February 2026. Results: Results showed uniform relationships among neurological conditions, loss of microbial richness, loss of short-chain fatty acid-producing bacteria, neuroinflammation, and nutritional susceptibility. The review also identifies methodological trends in microbiome profiling and nutritional assessment and suggests an integrative framework of symptom-linked microbial imbalance, malnutrition, and inflammatory processes. Conclusions: Although dietary modulation and microbiome-targeted interventions appear promising, the evidence is mostly correlational. Longitudinal and interventional studies should be well-designed to elucidate causal mechanisms and to provide effective clinical strategies.},
}

@article {pmid42123326,
year = {2026},
author = {Zaman, S and Ali, N and Ullah, W and Taimur, N and Akbar, NU and Waheed, A and Muhammad, N and Khan, MS},
title = {Metagenomic Profiling Reveals Extensive Bacterial Diversity in Chicken Manure and Associated Contaminated Wastewater.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123326},
issn = {1422-0067},
mesh = {Animals ; Chickens/microbiology ; *Manure/microbiology ; *Wastewater/microbiology ; *Metagenomics/methods ; *Bacteria/genetics/classification/isolation & purification ; Metagenome ; Microbiota/genetics ; Biodiversity ; },
abstract = {Chicken manure and its potential to contaminate water systems through the dispersal of pathogenic bacteria are major concerns in environmental and public health. In this study, a metagenomic analysis was employed to systematically identify and compare bacterial assemblages in chicken manure (CM) and in a contaminated sample of chicken manure wastewater (CMW). Whole DNA was extracted from CM and CMW, followed by whole-genome shotgun sequencing; data analysis was done using online Galaxy software (ver. 26.0.1.dev1). Metagenomic analysis reveals a complex One Health challenge. Data showed that CM and CMW are different in their microbiota, as indicated by a distinct separation of beta diversity values and limited overlapping of species between sample types. In the current study, we found a greatly significant common functional set of adapted bacterial masses, including major pathogenic bacterial groups as well as opportunistic and environmental bacterial species, indicative of a direct contamination from CM and CMW. Notably, in both CM and CMW, a plethora of opportunistic, enteric, and environmental pathogens like Escherichia coli, Salmonella enterica, and Acinetobacter baumannii were found, coupled with an indication of a direct functional flow between both ecosystems as tangled reservoirs. Chicken manure samples showed differences in taxonomic composition and inferred functional profiles at the time of sampling: CM1 was pathogen-enriched, CM2 exhibited strong nitrogen-supportive metabolism, CM3 was dominated by fiber-degrading decomposers, and CM4 showed high methane-producing potential with environmental risk. Such findings underscore the raising of chickens as a potential source of harmful bacteria for the environment. It is important to note that this study represents a preliminary investigation with certain limitations, including the absence of biological replicates, lack of temporal sampling, and limited capacity to infer dynamic ecological interactions. Yet this metagenomic report is more about describing the taxonomy and functional potential of the bacteria, rather than discussing the actual ecological processes of these microorganisms in the environment. Future studies will be required to explore these aspects.},
}

Animals
Chickens/microbiology
*Manure/microbiology
*Wastewater/microbiology
*Metagenomics/methods
*Bacteria/genetics/classification/isolation & purification
Metagenome
Microbiota/genetics
Biodiversity

@article {pmid42123347,
year = {2026},
author = {López-Tenorio, II and Constantino-Jonapa, LA and Jaimez-Alvarado, S and Hernández-Quiroz, F and Jorge-Galarza, E and Escalona-Montaño, AR and Amedei, A and Soria-García, R and Berrios-Barcenas, EA and Aguirre-García, MM},
title = {Gut-Heart Axis: Microbiome Involvement in Wild-Type Transthyretin Amyloidosis.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123347},
issn = {1422-0067},
support = {CBF2023-2024-734//CONAHCYT/ ; IN212422, IN219025//UNAM-DGAPA-PAPIIT/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Amyloid Neuropathies, Familial/microbiology/metabolism ; Male ; Female ; Middle Aged ; Aged ; Biomarkers/metabolism ; Dysbiosis/microbiology ; },
abstract = {Cardiac amyloidosis is a rare and progressive condition characterized by the extracellular deposition of amyloid fibrils in multiple organs. Wild-type transthyretin amyloidosis (ATTR-wt) is the most common type affecting subjects above 60 years old. Recent and growing evidence suggests a potential link between GM and cardiac amyloidosis. In this scenario, the aim of the present study is to characterize the gut microbiota (GM), related metabolites and inflammatory biomarkers in ATTR-wt patients. In the ATTR patients we identified Prevotella_9 as the core OTUs (Operational Taxonomic Unit) of this group, alongside Prevotella 7, Prevotellaceae_UCG-003 and Prevotellaceae_NK3B31. In addition, there were increased levels of long fatty acids, including tetradecanoic, hexadecanoic and octadecanoic acids, in the ATTR group. The data obtained suggest that ATTR patients have an altered gut microbiota that could be used as a potential biomarker in metabolic and cardiovascular diseases, as well as a potential predictor of adverse prognosis in ATTR patients. In addition, the intestinal dysbiosis in ATTR patients could be associated with low-grade endotoxemia promoting a pro-inflammatory state due to the translocation of bacterial components, such as LPS (lipopolysaccharide), into blood circulation.},
}

Humans
*Gastrointestinal Microbiome
*Amyloid Neuropathies, Familial/microbiology/metabolism
Male
Female
Middle Aged
Aged
Biomarkers/metabolism
Dysbiosis/microbiology

@article {pmid42123418,
year = {2026},
author = {Bhoi, TK and Mahanta, DK and Samal, I and Jangra, S},
title = {Plant Defense Activation by Endophytic Metarhizium anisopliae and Beauveria bassiana Fungi Against Subterranean Termites.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123418},
issn = {1422-0067},
mesh = {Animals ; *Metarhizium/pathogenicity/physiology ; *Isoptera/microbiology ; *Beauveria/pathogenicity/physiology ; *Endophytes/physiology ; },
abstract = {Subterranean termites, particularly Odontotermes obesus, cause severe damage to forest nurseries and plantations in arid and semi-arid ecosystems. This study demonstrates the dual functional role of endophytic entomopathogenic fungi, Metarhizium anisopliae and Beauveria bassiana, in termite suppression and induction of plant defense responses. Laboratory bioassays revealed significantly higher virulence of M. anisopliae, with a lower LT50 (lethal time required to cause 50% mortality) of 33.1 h compared to B. bassiana (46.7 h), a steeper probit slope (5.4 ± 0.3), and strong model fit (R[2] = 0.95), indicating rapid and synchronized mortality. Endophytic colonization varied across host species and application methods, with soil incorporation consistently outperforming foliar inoculation. Maximum colonization (82.5%) was recorded in Tecomella undulata and exceeded 80% in Azadirachta indica under M. anisopliae. Biochemical analyses revealed significant increases in protein (up to 3.5 mg g[-1]), phenols (3.7 mg g[-1]), and tannins (2.7 mg g[-1]). Activity of defense enzymes was significantly enhanced, with catalase reaching 263.5 U mL[-1], while Phenylalanine ammonia-lyase and Tyrosine ammonia-lyase exceeded 170 and 198 U mL[-1], respectively, indicating activation of antioxidant and phenylpropanoid pathways. Molecular docking analysis further revealed strong interactions between fungal metabolites and termite cellulase, with Bassianin (-8.4 kcal mol[-1]) and Tenellin (-8.1 kcal mol[-1]) showing the highest binding affinities. These findings highlight the combined biochemical and molecular mechanisms underlying fungal-mediated termite suppression and plant defense induction, and future research should prioritize transcriptomic validation, rhizosphere microbiome interactions, formulation optimization, and long-term multi-location field evaluation to support sustainable termite management strategies.},
}

Animals
*Metarhizium/pathogenicity/physiology
*Isoptera/microbiology
*Beauveria/pathogenicity/physiology
*Endophytes/physiology

@article {pmid42123449,
year = {2026},
author = {Toboła, M and Kuryłowicz, A},
title = {Impact of Gut Microbiota on Bone Metabolism-Present Concepts and Therapeutic Implications.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123449},
issn = {1422-0067},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Bone and Bones/metabolism ; Animals ; Dysbiosis/metabolism/microbiology ; Probiotics/therapeutic use ; Calcium/metabolism ; Fatty Acids, Volatile/metabolism ; Prebiotics ; },
abstract = {The gut microbiota plays a multifaceted role in calcium homeostasis and bone metabolism -acting through metabolic, immunological, and hormonal pathways that collectively constitute the gut-bone axis. The microbiota influences calcium bioavailability through several overlapping mechanisms that act in the intestine. Moreover, microbial fermentation products may directly impact the osteoblast-osteoclast interplay and, by modulating immune and endocrine functions, are crucial for bone metabolism. A healthy microbiota supports bone formation; however, intestinal dysbiosis may impair bone structure and function. This narrative review aims to present pathways linking the gut microbiota to bone metabolism, both in health and disease. First, we will discuss the influence of gut microbiota on calcium absorption. We will then outline the role that microbial metabolites, such as bile acids and short-chain fatty acids (SCFAs), play in regulating bone structure and function. In the following section, we will discuss the role of the microbiota in the immunological and hormonal modulation of bone metabolism. Finally, we will discuss how dysbiosis affects bone and how therapeutic interventions, such as probiotics, prebiotics, and postbiotics, may influence bone tissue quality.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Bone and Bones/metabolism
Animals
Dysbiosis/metabolism/microbiology
Probiotics/therapeutic use
Calcium/metabolism
Fatty Acids, Volatile/metabolism
Prebiotics

@article {pmid42123477,
year = {2026},
author = {Baldo, E and Abeni, D and Agostini, G and Armato, U and Bauer, P and Belloni Fortina, A and Calza, A and Cervadoro, E and Chiarini, A and Ciprandi, G and Dal Prà, I and Faga, A and Farina, S and Geat, D and Giovannini, M and Girolomoni, G and Gisondi, P and Jousson, O and Manara, S and Mira, E and Nicoletti, G and Pagliarello, C and Pedron, R and Peroni, A and Rizzo, V and Segata, N and Tettamanti, G and Zanoni, M and Zumiani, G and Cristofolini, M},
title = {Clinical and Mechanistic Evidence for Comano Thermal Water: A Narrative Review.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123477},
issn = {1422-0067},
mesh = {Humans ; *Mineral Waters/therapeutic use ; Balneology/methods ; Animals ; Skin/drug effects ; },
abstract = {Comano thermal water (CTW) is a hypotonic, bicarbonate-calcium-magnesium mineral water traditionally used to manage chronic inflammatory and relapsing skin diseases. This review summarises and discusses the available clinical, experimental, and translational evidence on CTW, with a particular focus on dermatological indications. The physicochemical properties of CTW, along with the presence of a stable, non-pathogenic microbial community, are examined in relation to their potential biological activity. Clinical studies indicate that CTW-based balneotherapy, alone or in combination with narrowband Ultraviolet B (UVB) phototherapy, is associated with improvements in disease severity, symptom burden, and quality of life in patients with psoriasis and atopic dermatitis, and has a favourable safety and tolerability profile. Experimental data further suggest that CTW may exert anti-inflammatory and immunomodulatory effects, modulate keratinocyte function, support skin barrier restoration, and influence the cutaneous microenvironment, including microbiome-related pathways. The review also outlines emerging evidence for CTW in skin regeneration and in upper airway inflammatory conditions treated via inhalation-based approaches. Overall, this review suggests that CTW may serve as a biologically active therapeutic resource, warranting further investigation as a complementary approach within integrative management strategies for inflammatory and barrier-related conditions.},
}

Humans
*Mineral Waters/therapeutic use
Balneology/methods
Animals
Skin/drug effects

@article {pmid42123484,
year = {2026},
author = {Ahmad, A and Ahmed, MM and Akhtar, A and Liu, W and Yang, R and Sun, X and Wang, X and Bibi, S and Khan, MB and Chen, S},
title = {Unlocking Grass Stress Resistance: Fungal Endophyte-Mediated Pathogen Recognition and RNA Regulation.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123484},
issn = {1422-0067},
support = {32260356//National Natural Science Foundation of China/ ; (Outstanding Youth Project, Grant No. 2025DB003)//Corps Science and Technology Program/ ; (TDZKPY202607)//Tarim University of Agricultural Reclamation/ ; },
mesh = {*Endophytes/physiology ; *Stress, Physiological ; *Poaceae/microbiology/genetics/physiology ; *Host-Pathogen Interactions ; Symbiosis ; *Fungi/physiology ; Gene Expression Regulation, Plant ; Disease Resistance ; Plant Diseases/microbiology/genetics ; },
abstract = {Fungal endophytes are symbiotic microorganisms that establish strong relationships inside plant tissues, providing potential advantages, especially in grasses, by enhancing tolerance to both abiotic and biotic stresses. This review investigates the molecular mechanisms through which fungal endophytes mediate stress tolerance, targeting host-pathogen interactions. By modulating pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), and effector proteins, fungal endophytes may contribute to priming the plant's immune system, enhancing its resistance to pathogen invasion. Moreover, endophyte colonization regulates core processes such as osmotic regulation, reactive oxygen species (ROS) detoxification, and secondary metabolite biosynthesis that enable plants to tolerate environmental stresses like drought, heat, and salinity. The review highlights the impact of endophytes on immune priming, systemic acquired resistance (SAR), and the regulation of non-coding RNAs that regulate host gene networks associated with stress tolerance. Furthermore, the integration of advanced multi-omics techniques genomics, transcriptomics, proteomics, metabolomics, and fluxomics has revealed emerging insights into the genetic and metabolic pathways driving these symbiotic associations. However, grass-specific molecular datasets remain limited, and the consistency of endophyte-mediated tolerance across host species and environmental conditions is not yet fully resolved. Fungal endophytes increase grass stress resilience through coordinated pathogen recognition, RNA regulation, and metabolic reprogramming while AI-assisted multi-omics approaches are emerging as tools for identifying candidate regulatory networks, although empirical validation in grass-endophyte systems remains limited. Together, these advances highlight the potential for climate-smart and sustainable crop improvement. Future research integrating functional genomics, field validation, and biosafety assessment will be essential for translating endophyte-based strategies into reliable agricultural applications.},
}

*Endophytes/physiology
*Stress, Physiological
*Poaceae/microbiology/genetics/physiology
*Host-Pathogen Interactions
Symbiosis
*Fungi/physiology
Gene Expression Regulation, Plant
Disease Resistance
Plant Diseases/microbiology/genetics

@article {pmid42123517,
year = {2026},
author = {Nguyen-DeMary, K and Vascellari, S and Mastinu, M and Melis, M and Bastiaanssen, TFS and Tomassini Barbarossa, I and Tepper, BJ},
title = {Cranberry Polyphenol Extract (CPE) Oral Rinse Improves Salivary Microbiome in 6-n-Propylthiouracil (PROP) Non-Tasters and Palatability of Aronia Juice.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123517},
issn = {1422-0067},
support = {10180//United States Department of Agriculture/ ; },
mesh = {Humans ; *Saliva/microbiology/drug effects ; Female ; Male ; *Vaccinium macrocarpon/chemistry ; *Polyphenols/pharmacology/administration & dosage/chemistry ; *Microbiota/drug effects ; Adult ; Propylthiouracil ; *Plant Extracts/pharmacology/chemistry/administration & dosage ; *Photinia/chemistry ; Taste/drug effects ; *Mouthwashes/pharmacology/chemistry ; *Fruit and Vegetable Juices ; Young Adult ; },
abstract = {Sensitivity to the bitterness of 6-n-propylthiouracil (PROP) is controlled by variations in the TAS2R38 gene. This phenotype is often used as a marker for individual differences in taste perception. Previous findings show that PROP taster status is associated with differences in the salivary microbiome. It is well known that diet and environmental factors influence the risk of oral disease, but there is far less evidence showing how genetic differences play a role. Forty-seven young, healthy, PROP taster-classified adults rinsed with a cranberry polyphenol extract (CPE) oral rinse (0.75 g/L CPE powder in spring water) twice daily for 11 days. Saliva was collected pre- and post-intervention for microbiome analysis using shotgun metagenomic sequencing. At the same time points, participants evaluated two astringent juices (cranberry and aronia berry) for key attributes. At baseline, PROP taster groups differed in their salivary microbiome compositions, but post-intervention, the groups had more similar bacterial compositions. Post-intervention, non-tasters showed decreases in the relative abundance of 15 bacterial species, including a significant reduction (p = 0.037) in Eikenella corrodens, which is one bacterium, among several others, involved in oral biofilm formation. Additionally, after the intervention, sourness was reduced, and overall liking increased significantly for aronia juice. Oral dysbiosis, a risk factor for oral disease, may be controlled by bactericidal mouthwashes. Our results suggest that CPE, a natural alternative to traditional bactericidal rinses, may selectively target pathobionts while preserving salivary microbiota diversity. CPE might also provide greater benefits to non-tasters, who are at greater risk for oral disease.},
}

Humans
*Saliva/microbiology/drug effects
Female
Male
*Vaccinium macrocarpon/chemistry
*Polyphenols/pharmacology/administration & dosage/chemistry
*Microbiota/drug effects
Adult
Propylthiouracil
*Plant Extracts/pharmacology/chemistry/administration & dosage
*Photinia/chemistry
Taste/drug effects
*Mouthwashes/pharmacology/chemistry
*Fruit and Vegetable Juices
Young Adult

@article {pmid42123520,
year = {2026},
author = {Yılmaz, A and Park, HJ and Ahn, EM and Bae, J},
title = {Dietary Polyphenols in Aging: A Systems-Level Perspective on Mitochondrial Quality Control and Microbiome Interactions.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123520},
issn = {1422-0067},
support = {RS-2026-25477916//National Research Foundation of Korea/ ; 2026-rise-15-110//Daegu Haany University Regional Innovation System & Education/ ; },
mesh = {Humans ; *Polyphenols/pharmacology ; *Aging/drug effects/metabolism ; *Mitochondria/metabolism/drug effects ; Animals ; *Gastrointestinal Microbiome/drug effects ; Diet ; Signal Transduction/drug effects ; },
abstract = {Aging is a multifactorial biological process characterized by progressive functional decline and increased susceptibility to chronic diseases. Targeting the molecular mechanisms underlying aging has therefore emerged as an important strategy for promoting healthy aging. Natural polyphenols, widely present in fruits, vegetables, tea, and medical and aromatic plants, have attracted considerable attention due to their geroprotective properties. This review examines current evidence on the ability of major dietary polyphenols, including resveratrol, epigallocatechin gallate (EGCG), curcumin, and quercetin, to modulate the hallmarks of aging, with particular emphasis on mitochondrial quality control as a central regulatory mechanism. Evidence indicates that polyphenols regulate key signaling pathways involved in aging biology, including AMP-activated protein kinase (AMPK), sirtuins (SIRT), mechanistic target of rapamycin (mTOR), nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-κB (NF-κB). Through coordinated modulation of these pathways, polyphenols influence mitochondrial biogenesis, mitophagy, redox homeostasis, cellular senescence, and chronic inflammation. In addition, interactions between dietary polyphenols and the gut microbiome generate bioactive metabolites, such as urolithin A, which further contribute to mitochondrial regulation. Overall, polyphenols represent promising modulators of aging-associated pathways and may support strategies aimed at improving healthspan and reducing age-related disease risk.},
}

Humans
*Polyphenols/pharmacology
*Aging/drug effects/metabolism
*Mitochondria/metabolism/drug effects
Animals
*Gastrointestinal Microbiome/drug effects
Diet
Signal Transduction/drug effects

@article {pmid42123539,
year = {2026},
author = {Miranda, J and Maestre, N and Devia, M and Zapata, R and Ochoa-Díaz, MM and Annicchiarico, W},
title = {Inflammation at the Maternal-Fetal Interface: Mechanisms Linking Maternal-Fetal Immunity to Preeclampsia and Fetal Growth Restriction.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123539},
issn = {1422-0067},
mesh = {Humans ; Pregnancy ; Female ; *Fetal Growth Retardation/immunology/pathology/etiology ; *Pre-Eclampsia/immunology/pathology ; *Inflammation/immunology/pathology ; *Placenta/immunology ; *Maternal-Fetal Exchange/immunology ; Animals ; },
abstract = {Inflammation is a physiological and tightly regulated component of normal pregnancy, contributing to implantation, placental development, and the initiation of parturition. The placenta functions as an active immunological hub, coordinating innate and adaptive immune responses to maintain tolerance while protecting against infection. Preeclampsia and fetal growth restriction (FGR) are major causes of maternal and perinatal morbidity worldwide and represent central manifestations of placental disease. Increasing evidence indicates that these conditions share key pathophysiological mechanisms, including placental dysfunction and maladaptive maternal immune responses. When immune regulation at the maternal-fetal interface becomes disrupted, inflammatory pathways contribute to impaired placental development and vascular maladaptation. In this context, excessive immune activation-driven by inflammasome signaling, Th1/Th17 polarization, and altered natural killer and macrophage function-can compromise placental perfusion, promote antiangiogenic imbalance, and lead to systemic endothelial dysfunction. This review, therefore, focuses on how immune dysregulation contributes to placental dysfunction in preeclampsia and FGR, synthesizing current knowledge of the maternal-fetal immune interface and exploring therapeutic strategies that link pathogenic mechanisms to targeted interventions. A deeper understanding of placental immunology and inflammatory signaling is essential to develop precision therapies. Established therapies, including low-dose aspirin, low-molecular-weight heparin, and antenatal corticosteroids, aim to mitigate inflammation and optimize fetal outcomes, while adjunctive strategies target oxidative stress, nutritional deficits, and the maternal microbiome. Emerging approaches such as cytokine-targeted biologics, inflammasome inhibitors, and mesenchymal stem cell therapies show promise but require rigorous safety and efficacy evaluation. Future research should prioritize biomarker validation, pathway-specific interventions, and equitable implementation to reduce inflammation-driven pregnancy complications.},
}

Humans
Pregnancy
Female
*Fetal Growth Retardation/immunology/pathology/etiology
*Pre-Eclampsia/immunology/pathology
*Inflammation/immunology/pathology
*Placenta/immunology
*Maternal-Fetal Exchange/immunology
Animals

@article {pmid42123569,
year = {2026},
author = {Osredkar, J and Fabjan, T and Godnov, U and Jekovec-Vrhovšek, M and Osredkar, D and Finderle, P and Kumer, K and Zorec, M and Fanedl, L and Avguštin, G},
title = {Microbiome-Derived Short-Chain Fatty Acids and Tryptophan Metabolites in Children with Autism Spectrum Disorder: A Stool-Urine Multi-Omics Analysis.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123569},
issn = {1422-0067},
support = {This research was funded by the scientific-research program grants P3-0124 and project J3-1756//The Slovenian Research and Innovation Agency/ ; },
mesh = {Humans ; *Tryptophan/metabolism/urine ; *Autism Spectrum Disorder/metabolism/microbiology/urine ; Male ; *Fatty Acids, Volatile/metabolism/urine ; Female ; *Feces/chemistry/microbiology ; Child ; *Gastrointestinal Microbiome ; Child, Preschool ; Metabolomics/methods ; Cross-Sectional Studies ; Case-Control Studies ; Metabolome ; Multiomics ; },
abstract = {Autism spectrum disorder (ASD) has been associated with alterations in the gut microbiota and its metabolites, particularly short-chain fatty acids (SCFAs) and microbiota-derived tryptophan catabolites, which may influence neurodevelopment through immune and epigenetic mechanisms. We investigated whether stool SCFAs and tryptophan-pathway metabolites differ between children with ASD and typically developing controls, and whether these metabolites associate with ASD severity and systemic biochemical signatures. In this cross-sectional study, we analyzed stool samples from 229 children (160 with ASD, 69 controls) with complete SCFA and tryptophan-metabolite data, while urine metabolomics data were available for a subset and were used for exploratory stool-urine integration analyses. Children with ASD and controls were similar in age, but the ASD group had a higher proportion of males. Absolute concentrations of individual SCFAs, total SCFAs, and derived indices were broadly comparable between groups; nominal differences in propionate/acetate ratio and caproate did not remain significant after false discovery rate correction. Similarly, stool tryptophan-pathway metabolites reported as ng/a.u. based on the NanoDrop-derived proxy (tryptophan, kynurenine, indole-3-acetic, indole-3-lactic, indole-3-propionic, indole-3-aldehyde, N-acetyl-tryptophan, serotonin, melatonin, tryptamine) and functional ratios (kynurenine/tryptophan, indole-derived/tryptophan, serotonin/tryptophan) showed no robust ASD-control differences; N-acetyl-tryptophan was nominally higher in ASD but did not survive multiple-testing correction. In the ASD subgroup with available Childhood Autism Rating Scale (CARS) data (n = 34), SCFA and tryptophan indices showed only weak, non-significant correlations with global ASD severity. In contrast, correlation analyses revealed two coherent metabolic modules, i.e., an SCFA block with very strong internal correlations among individual SCFAs and total SCFAs and a tryptophan block with strong correlations between metabolites and their normalized ratios, while cross-module correlations were modest. These results indicate that stool SCFA and microbiota-derived tryptophan profiles do not robustly distinguish ASD from controls in this cohort, but they form stable metabolic modules compatible with microbiome-epigenome frameworks.},
}

Humans
*Tryptophan/metabolism/urine
*Autism Spectrum Disorder/metabolism/microbiology/urine
Male
*Fatty Acids, Volatile/metabolism/urine
Female
*Feces/chemistry/microbiology
Child
*Gastrointestinal Microbiome
Child, Preschool
Metabolomics/methods
Cross-Sectional Studies
Case-Control Studies
Metabolome
Multiomics

@article {pmid42123593,
year = {2026},
author = {Sibarani, JN and Iqhrammullah, M and Hidayat, AA and Alfaray, RI and Nurkolis, F and Santini, A},
title = {Multi-Axis Reprogramming of Muscle-Metabolic Crosstalk by HiLo Platinum™ Restores Strength in Prediabetes via Mitochondrial Activation and Gut Microbiome Remodeling.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123593},
issn = {1422-0067},
mesh = {Animals ; Male ; *Gastrointestinal Microbiome/drug effects ; Rats ; Rats, Sprague-Dawley ; *Prediabetic State/metabolism/drug therapy ; *Muscle, Skeletal/metabolism/drug effects ; *Muscle Strength/drug effects ; *Mitochondria/metabolism/drug effects ; Biomarkers/metabolism ; Dietary Supplements ; Sarcopenia/metabolism ; Disease Models, Animal ; },
abstract = {Prediabetes is increasingly recognized as a risk factor for sarcopenia, driven by chronic low-grade inflammation, insulin resistance, and impaired anabolic signaling. Nutritional interventions containing whey protein, hydroxymethylbutyrate (HMB), glucosamine, and micronutrients may offer a multi-target strategy to counteract muscle deterioration. This study aimed to evaluate the efficacy of HiLo Platinum™ supplementation in attenuating muscle strength decline in a prediabetic rat model, with integrated analysis of metabolic biomarkers and gut microbiome profiles. A randomized preclinical trial was conducted using male Sprague Dawley rats assigned to four groups: normal diet (ND), prediabetic control induced by cholesterol- and fat-enriched diet with fructose (CFEDF), and two treatment groups receiving low-dose (0.63 g/kg BW) or high-dose (1.26 g/kg BW) HiLo Platinum™. The intervention lasted six weeks. Muscle strength was assessed via a four-limb grip strength test (reverse hang time and holding impulse). Biomarkers related to inflammation, mitochondrial function, and anabolic signaling (TNF-α, IL-10, PGC-1α, IGF-1, SIRT-1, AMPK, mTOR, and myostatin), lipid profile, and blood glucose were analyzed. Gut microbiome composition and diversity were evaluated using taxonomic profiling and multivariate analyses. HiLo Platinum™ supplementation significantly improved muscle strength, evidenced by increased reverse hang time and holding impulse (p < 0.001). Both doses reduced blood glucose and improved lipid profiles, including increased HDL and decreased LDL, triglycerides, and total cholesterol. Anti-inflammatory effects were observed with reduced TNF-α and elevated IL-10 levels. Mitochondrial and metabolic regulators (PGC-1α, SIRT-1, AMPK) and anabolic mediators (IGF-1) were significantly upregulated, while mTOR levels decreased. Gut microbiome analysis revealed increased genus richness (Chao1 index) and distinct microbial shifts associated with improved metabolic and inflammatory markers. HiLo Platinum™ effectively mitigates prediabetes-induced muscle strength decline through integrated modulation of inflammatory pathways, mitochondrial function, metabolic homeostasis, and gut microbiome composition. These findings support its potential as a nutritional therapeutic strategy for preventing sarcopenia in prediabetic conditions, although further studies are needed to evaluate long-term effects and implications on muscle hypertrophy.},
}

Animals
Male
*Gastrointestinal Microbiome/drug effects
Rats
Rats, Sprague-Dawley
*Prediabetic State/metabolism/drug therapy
*Muscle, Skeletal/metabolism/drug effects
*Muscle Strength/drug effects
*Mitochondria/metabolism/drug effects
Biomarkers/metabolism
Dietary Supplements
Sarcopenia/metabolism
Disease Models, Animal

@article {pmid42123679,
year = {2026},
author = {Chu, Y and Huang, KH and Tseng, CN},
title = {Targeting the Gut-Heart Axis in Diabetic Heart Failure: Microbiota and SGLT2is as Converging Therapeutic Frontiers.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123679},
issn = {1422-0067},
support = {From Chang Gung Memorial Hospital, Linkou Branch, Taiwan. (CMRPG3F1831, CMRPG3F1832, CMRPG3H0991, CMRPG3H0992, CMRPG3H1801, CMRPG3K0051, CMRPG3K0052, CMRPG3K0221, CMRPG3K0222,CMRPG3K1901,CMRPG3M0121) and from National Science and Technology Council, Taiwa//Linkou Chang Gung Memorial Hospital/ ; },
mesh = {Humans ; *Sodium-Glucose Transporter 2 Inhibitors/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/drug effects ; *Heart Failure/drug therapy/metabolism/etiology/microbiology ; *Diabetes Mellitus, Type 2/drug therapy/complications/microbiology/metabolism ; Animals ; Fatty Acids, Volatile/metabolism ; },
abstract = {Emerging evidence highlights the gut microbiota as a critical modulator in the pathogenesis of heart failure (HF), particularly among patients with type 2 diabetes mellitus (T2DM). Dysbiosis contributes to systemic inflammation, endothelial dysfunction, and adverse cardiac remodeling via microbial metabolites such as trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs). However, the therapeutic intersection between the gut microbiota and pharmacological interventions remains insufficiently integrated. Sodium-glucose cotransporter-2 inhibitors (SGLT2is), a cornerstone of T2DM management, confer cardioprotective effects that may involve microbiota-mediated pathways. This review provides a novel synthesis of how SGLT2is influence gut ecology, specifically through altered glucose excretion and osmotic shifts, to potentially restore SCFA-producing taxa. By delineating the structural transitions from gut physiology to SGLT2i-modulated cardiac outcomes, we emphasize the gut-heart axis as a pivotal therapeutic target. This focused framework offers new insights into the triadic interplay between microbiome stability and cardiometabolic health, moving beyond traditional glucose-centric paradigms.},
}

Humans
*Sodium-Glucose Transporter 2 Inhibitors/therapeutic use/pharmacology
*Gastrointestinal Microbiome/drug effects
*Heart Failure/drug therapy/metabolism/etiology/microbiology
*Diabetes Mellitus, Type 2/drug therapy/complications/microbiology/metabolism
Animals
Fatty Acids, Volatile/metabolism

@article {pmid42123693,
year = {2026},
author = {Seifert, O and Assarsson, M and Manoharan, L and Söderman, J},
title = {Integrated Host Genetics and Skin Microbiome Profiling Suggest an HLA-C-Peptostreptococcus Axis in Psoriasis.},
journal = {International journal of molecular sciences},
volume = {27},
number = {9},
pages = {},
pmid = {42123693},
issn = {1422-0067},
support = {FUTURUM-1012326, FUTURUM-996859, and FUTURUM-1006909//Futurum - Akademin för Hälsa och Vård/ ; N/A//Swedish Psoriasis Association/ ; },
mesh = {Humans ; *Psoriasis/genetics/microbiology/immunology ; *Skin/microbiology ; *Microbiota/genetics ; Polymorphism, Single Nucleotide ; Male ; *HLA-C Antigens/genetics ; Female ; Genetic Predisposition to Disease ; Adult ; Middle Aged ; RNA, Ribosomal, 16S/genetics ; Genotype ; Case-Control Studies ; Skin Microbiome ; },
abstract = {Psoriasis is a chronic immune-mediated disease driven by genetic susceptibility and environmental factors, including microbial exposure. While HLA-C-linked variants represent the strongest genetic risk factors, their relationship with the cutaneous microbiome remains incompletely understood. This study aimed to investigate host-microbiome interactions in psoriasis through integrative multi-omics analysis. Skin microbiome profiling using 16S rRNA sequencing and targeted genotyping of psoriasis-associated single-nucleotide polymorphisms (SNPs) was performed in lesional and non-lesional skin from patients with plaque psoriasis and in healthy controls. Integrated analysis was conducted using supervised multivariate modeling (DIABLO) to identify coordinated genetic and microbial features associated with disease status. Combined genetic and microbial signatures differentiated lesional, non-lesional, and healthy skin. Variants within the HLA-C susceptibility region, including rs12191877, rs10484554, and rs4406273, showed contributions to group separation and demonstrated positive associations with Peptostreptococcus anaerobius. Associations involving ERAP1 variants linked antigen-processing pathways with inflammation-associated microbial taxa in lesional skin. Importantly, genotype-microbiome correlations were also detected in clinically non-lesional skin, where an increased psoriasis risk allele dosage co-varied with a higher relative abundance of P. anaerobius and Aerococcus urinae. In contrast, commensal-associated taxa were enriched in healthy controls and formed genotype-linked clusters only in non-lesional skin. These findings suggest that psoriasis is characterized by coordinated host genetic and microbial interaction patterns centered on antigen presentation pathways. The presence of a genotype-microbiome coupling in non-lesional skin may indicate that genetically determined immune configurations could shape microbial community structure prior to visible lesion development. Rather than reflecting uniform dysbiosis, psoriasis may represent a dynamic host-microbe ecosystem in which genetic susceptibility influences microbial persistence and inflammatory readiness.},
}

Humans
*Psoriasis/genetics/microbiology/immunology
*Skin/microbiology
*Microbiota/genetics
Polymorphism, Single Nucleotide
Male
*HLA-C Antigens/genetics
Female
Genetic Predisposition to Disease
Adult
Middle Aged
RNA, Ribosomal, 16S/genetics
Genotype
Case-Control Studies
Skin Microbiome

@article {pmid42123776,
year = {2026},
author = {Wang, M and Zhu, L and Liao, J and Bao, L and Li, H and Deng, Z and Li, J and Zheng, L and Zhang, B},
title = {Human Milk Oligosaccharide LNnT Attenuates Colonic Barrier Dysfunction and Associated Cognitive Impairment via Modulating Sphingolipid Metabolism and Gut Microbiota.},
journal = {Molecules (Basel, Switzerland)},
volume = {31},
number = {9},
pages = {},
pmid = {42123776},
issn = {1420-3049},
support = {No.82560639//National Natural Science Foundation of China/ ; No.20252BAC250147//Key Project of Natural Science Foundation of Jiangxi Province/ ; },
mesh = {*Gastrointestinal Microbiome/drug effects ; Animals ; Mice ; Humans ; *Sphingolipids/metabolism ; *Cognitive Dysfunction/metabolism/drug therapy ; *Milk, Human/chemistry ; *Oligosaccharides/pharmacology/chemistry ; *Colon/drug effects/metabolism/pathology ; Male ; Galactose ; Intestinal Mucosa/metabolism/drug effects ; Oxidative Stress/drug effects ; Disease Models, Animal ; Mice, Inbred C57BL ; },
abstract = {This study focuses on Lacto-N-neotetraose (LNnT), a core component of human milk oligosaccharides. Although LNnT has been demonstrated to promote early intestinal development and maintain gut homeostasis, its protective mechanism against D-galactose-induced intestinal injury and associated cognitive impairment remains unclear. This investigation systematically examined the protective effects and underlying mechanisms of LNnT against D-gal-induced colonic damage and cognitive impairment in mice. The results demonstrated that LNnT not only significantly improved systemic physiological phenotypes and upregulated the expression of colonic tight junction proteins to repair the intestinal barrier, but also effectively enhanced learning and memory abilities in mice. Concurrently, LNnT reduced serum proinflammatory factor levels, elevated the anti-inflammatory factor IL-10, and alleviated oxidative stress. Furthermore, LNnT remodeled the gut microbiome structure by increasing microbial diversity, enhancing beneficial bacteria abundance, and promoting short-chain fatty acid production. Untargeted metabolomics analysis further revealed that LNnT corrected metabolic disturbances by regulating key sphingolipid molecules (ceramide, sphingosine, S1P) and the expression of related metabolic enzymes (ACER2, SphK2). In summary, this study suggests that LNnT mitigates intestinal injury and improves cognitive function, potentially through modulation of the gut microbiota-sphingolipid metabolism axis, although further causal validation is warranted. These findings provide a mechanistic foundation for future studies exploring its potential as a functional dietary ingredient.},
}

*Gastrointestinal Microbiome/drug effects
Animals
Mice
Humans
*Sphingolipids/metabolism
*Cognitive Dysfunction/metabolism/drug therapy
*Milk, Human/chemistry
*Oligosaccharides/pharmacology/chemistry
*Colon/drug effects/metabolism/pathology
Male
Galactose
Intestinal Mucosa/metabolism/drug effects
Oxidative Stress/drug effects
Disease Models, Animal
Mice, Inbred C57BL

@article {pmid42123920,
year = {2026},
author = {Hachmeriyan, A and Panayotova, G and Todorova, H},
title = {From Plate to Mind: Scientific Perspectives on Foods That May Influence Anxiety and Depression.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42123920},
issn = {2072-6643},
mesh = {Humans ; *Fatty Acids, Omega-3/administration & dosage ; *Depression/diet therapy ; *Anxiety/diet therapy ; Gastrointestinal Microbiome ; Micronutrients/administration & dosage ; Dietary Supplements ; *Diet ; Randomized Controlled Trials as Topic ; Brain ; Probiotics/administration & dosage ; Vitamins/administration & dosage ; },
abstract = {Background: Nutritional psychiatry increasingly links diet quality and specific bioactive nutrients to depression and anxiety outcomes. Mechanistic evidence implicates neuroimmune activation, inflammation, altered neurotransmitter synthesis, and microbiota-derived metabolites. Objective: The objective of this study is to synthesize evidence on omega-3 polyunsaturated fatty acids (n-3 PUFAs), the microbiota-gut-brain axis, and vitamins and minerals that influence neurotransmitter synthesis, inflammation, and brain function and to translate these findings into food-based strategies. Methods: This study consisted of a focused synthesis of randomized controlled trials (RCTs), meta-analyses, and systematic reviews indexed in PubMed, Scopus and Web of Science, selected for relevance to omega-3s, probiotics/prebiotics, dietary patterns, and micronutrients (folate/B-vitamins, vitamin D, magnesium, zinc, and vitamin C/copper pathways). Results: RCT and meta-analytic evidence suggest modest benefits of omega-3 supplementation for anxiety severity and depressive symptoms, with heterogeneity by dose, EPA: DHA composition, and baseline inflammatory status. The gut-brain axis literature supports bidirectional effects of stress and microbiota, and meta-analyses of probiotics/prebiotics show small improvements in depressive and anxiety symptoms, likely dependent on strain and host phenotype. Micronutrients serve as enzymatic cofactors for monoamine and GABA synthesis and modulate immune signaling; clinical effects are the most consistent when correcting insufficiency or in biomarker-defined subgroups. A whole-diet RCT demonstrates that structured dietary improvement can reduce depressive symptoms as adjunctive therapy. Conclusions: A food-first approach emphasizing Mediterranean-style dietary patterns, omega-3-rich seafood, a diverse array of fiber, and micronutrient density is the most defensible. Supplementation may be considered selectively, guided by clinical context and nutritional status.},
}

Humans
*Fatty Acids, Omega-3/administration & dosage
*Depression/diet therapy
*Anxiety/diet therapy
Gastrointestinal Microbiome
Micronutrients/administration & dosage
Dietary Supplements
*Diet
Randomized Controlled Trials as Topic
Brain
Probiotics/administration & dosage
Vitamins/administration & dosage

@article {pmid42123927,
year = {2026},
author = {Rodziewicz, A and Bryl, E},
title = {The Role of Microbiome and Diet on Disease Activity and Immune-Inflammatory Status in Rheumatoid Arthritis.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42123927},
issn = {2072-6643},
support = {01-10026/0010451/01/262/0/2026//Gdańsk Medical University/ ; },
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology/diet therapy/prevention & control ; *Gastrointestinal Microbiome ; *Diet ; Probiotics/administration & dosage ; Diet, Mediterranean ; Dietary Supplements ; Inflammation ; Prebiotics ; },
abstract = {Rheumatoid arthritis (RA) is a chronic inflammatory disease of autoimmune background and unknown etiology. The importance of genetic factors in RA development is well-established. Environmental factors have also been extensively researched in relation to risk of RA and managing its symptoms. Smoking, physical activity, diet, and gut microbiota are considered to be the most essential modifiable factors in RA. Among dietary interventions, the most researched is Mediterranean diet, monounsaturated fatty acids, fish consumption, and fish oil (EPA, eicosapentaenoic acid and DHA, that is, docosahexaenoic acid). Others concerned gluten-free and vegan or vegetarian diet, salt intake, supplementation with vitamin D, antioxidants, prebiotics, and probiotics. Diet modifications can alter the gut environment, and the association between RA development or severity and the composition of gut bacteria has already been shown. This review focuses on effectiveness and usefulness of various dietary approaches and supplements in RA prevention and management, including the influence on disease activity and inflammatory status. The composition of gut microbiota and its changes in response to dietary factors are also considered. There is a great need for further research into mutual dependencies of diet, microbiome, and RA activity. The current state of knowledge provides promising evidence for future nutrition and microbial therapies.},
}

Humans
*Arthritis, Rheumatoid/immunology/microbiology/diet therapy/prevention & control
*Gastrointestinal Microbiome
*Diet
Probiotics/administration & dosage
Diet, Mediterranean
Dietary Supplements
Inflammation
Prebiotics

@article {pmid42123931,
year = {2026},
author = {Maragno, P and Amoroso, C and Conforti, S and Michelon, M and Honcharyuk, I and Ciafardini, C and Noviello, D and Strati, F and Caprioli, F and Facciotti, F and Vecchi, M},
title = {The Assessment of Multidimensional Clinical, Biological and Patient-Reported Outcomes to Evaluate the Efficacy of Add-On Lactobacillus rhamnosus GG Supplementation in Mild Ulcerative Colitis: A Randomized Pilot Trial.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42123931},
issn = {2072-6643},
mesh = {Humans ; *Colitis, Ulcerative/therapy/drug therapy/microbiology ; Pilot Projects ; Female ; Male ; *Lacticaseibacillus rhamnosus ; Adult ; Double-Blind Method ; Middle Aged ; Mesalamine/therapeutic use/administration & dosage ; *Probiotics/administration & dosage/therapeutic use ; *Dietary Supplements ; Patient Reported Outcome Measures ; Quality of Life ; Gastrointestinal Microbiome/drug effects ; Treatment Outcome ; *Cholecalciferol/administration & dosage/therapeutic use ; Leukocyte L1 Antigen Complex/analysis ; Feces/chemistry/microbiology ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; },
abstract = {Background: Ulcerative colitis (UC) is a multifactorial disease characterized by aberrant mucosal immune activation in response to intestinal dysbiosis. Contemporary management strategies aim to target inflammation and microbiome alterations while reducing relapse risk. A multidimensional assessment integrating clinical, inflammatory, immune, and microbial endpoints may better capture therapeutic effects beyond symptom control. Aims: To evaluate whether supplementation with Lactobacillus rhamnosus GG co-formulated with vitamin D3 (Dicoflor IBD Immuno) as an adjunct to optimized mesalamine (5-ASA) is associated with coordinated changes across clinical and biological domains in mild-to-moderate UC, using a multidimensional assessment framework. Methods: This single-center, randomized, double-blind, placebo-controlled pilot trial was conducted at Fondazione Ca' Granda IRCCS Policlinico di Milano between May 2022 and May 2024. Thirty-six patients with mild-to-moderate UC receiving optimized 5-ASA were randomized to LGG+VitD3 (ALD3) or placebo (AP) for 4 weeks. Clinical activity, health-related quality of life (HRQoL), fecal calprotectin, peripheral immune cell subsets, and gut microbiota composition were assessed at baseline and week 4. Results: Both 5-ASA-LGG+VitD3 (ALD3)- and 5-ASA-placebo (AP)-treated patients showed significant improvement in clinical activity and HRQoL, without between-group differences. A higher proportion of clinical responders was observed in the ALD3 group, although this was not statistically significant. LGG+VitD3-supplemented patients showed reduced fecal calprotectin levels and increased frequencies of IL-22-producing CD4[+] T cells. Microbiome analysis revealed enrichment of short-chain fatty acid-producing taxa, including Coprococcus and Fusicatenibacter, in ALD3-treated patients. Conclusions: In patients with mild UC receiving optimized 5-ASA, LGG+VitD3 supplementation does not improve short-term clinical outcomes beyond placebo but is associated with favorable modulation of inflammatory, immune, and microbial parameters, supporting the relevance of multidimensional biological endpoints in adjunctive UC management.},
}

Humans
*Colitis, Ulcerative/therapy/drug therapy/microbiology
Pilot Projects
Female
Male
*Lacticaseibacillus rhamnosus
Adult
Double-Blind Method
Middle Aged
Mesalamine/therapeutic use/administration & dosage
*Probiotics/administration & dosage/therapeutic use
*Dietary Supplements
Patient Reported Outcome Measures
Quality of Life
Gastrointestinal Microbiome/drug effects
Treatment Outcome
*Cholecalciferol/administration & dosage/therapeutic use
Leukocyte L1 Antigen Complex/analysis
Feces/chemistry/microbiology
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use

@article {pmid42123938,
year = {2026},
author = {Chiang, CK and Lai, CL and Chiu, MH and Huang, CJ},
title = {The Gut-Lung Axis in Allergic Asthma: A Narrative Review of Microbial Dysbiosis, Immune Regulation, and Nutritional Modulation.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42123938},
issn = {2072-6643},
support = {CGH-MR-B-11316//Cathay General Hospital/ ; },
mesh = {Humans ; *Dysbiosis/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; *Asthma/immunology/microbiology ; *Lung/immunology/microbiology ; Animals ; Diet ; },
abstract = {Allergic asthma is a prevalent chronic inflammatory disease of the airways whose pathogenesis has traditionally been attributed to localized immune dysfunction within the lung. However, accumulating evidence from microbiome research supports a broader system-level perspective in which cross-organ interactions contribute to disease susceptibility and progression. In particular, the gut-lung axis has emerged as a key regulatory pathway linking intestinal microbial ecology, immune development, and respiratory health. This review synthesizes current epidemiological, mechanistic, and experimental evidence supporting the role of gut microbiota dysbiosis in allergic asthma. We examine how early-life environmental and nutritional exposures and gut microbiota establishment during critical developmental windows shape long-term immune tolerance and asthma susceptibility. We then summarize characteristic features of asthma-associated gut dysbiosis and discuss how microbial-derived metabolites, including short-chain fatty acids, tryptophan metabolites, pro-allergic lipid mediators such as 12,13-dihydroxy-9Z-octadecenoic acid, and bacterial-derived histamine, modulate distal airway immune responses through epigenetic, receptor-mediated, and immune trafficking mechanisms. Particular emphasis is placed on the role of diet as a key upstream regulator of gut microbiota composition and metabolic function. Finally, we evaluate experimental and translational studies targeting the gut-lung axis, including dietary modulation, microbiome-targeted interventions such as fecal microbiota transplantation, and emerging postbiotic approaches. Collectively, current evidence indicates that gut microbial composition and metabolic function are critical determinants of respiratory immune homeostasis. Targeting the gut-lung axis through nutrition- and microbiome-based strategies offers a promising avenue for the prevention and precision treatment of allergic asthma.},
}

Humans
*Dysbiosis/immunology/microbiology
*Gastrointestinal Microbiome/immunology
*Asthma/immunology/microbiology
*Lung/immunology/microbiology
Animals
Diet

@article {pmid42123967,
year = {2026},
author = {Blady, K and Pomianowski, B and Smółka, L and Strugała, M and Kursa, K and Stanek, A},
title = {The Therapeutic Potential of Polyphenols in Modulating Barrier Lipids, Microbiome Interactions, and Inflammatory Pathways in Atopic Dermatitis.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42123967},
issn = {2072-6643},
mesh = {Humans ; *Polyphenols/pharmacology/therapeutic use ; *Dermatitis, Atopic/drug therapy/microbiology/metabolism ; Filaggrin Proteins ; Animals ; Gastrointestinal Microbiome/drug effects ; *Anti-Inflammatory Agents/pharmacology ; Inflammation/drug therapy ; *Lipid Metabolism/drug effects ; Epidermis/drug effects/metabolism ; Signal Transduction/drug effects ; *Microbiota/drug effects ; },
abstract = {Atopic dermatitis (AD) is a chronic inflammatory skin disease with a complex pathogenesis involving epidermal barrier dysfunction, microbiome dysbiosis, and immune dysregulation. Despite significant advances in therapy, including biologics and targeted treatments, their use may be limited by adverse effects, highlighting the need for safe adjunctive strategies. Polyphenols are naturally occurring bioactive compounds that are abundant in plant-based foods and are known for their anti-inflammatory, antioxidant, and immunomodulatory properties, making them promising candidates for supportive AD management. This review integrates current evidence on the effects of polyphenols on epidermal barrier lipids, microbiome interactions, and key inflammatory pathways, including NF-κB and JAK/STAT signaling. Additionally, the role of polyphenols in modulating dendritic cell and neutrophil activity, and reducing reactive oxygen species (ROS) production and neutrophil extracellular trap (NET) formation, as well as their potential involvement in mitophagy regulation, is discussed. Polyphenols support epidermal barrier integrity by modulating the expression of key structural proteins, including filaggrin, involucrin, and loricrin, leading to a reduction in transepidermal water loss (TEWL). Furthermore, they interact bidirectionally with the gut microbiome, acting as metabolic substrates for beneficial bacteria and promoting the growth of short-chain fatty acid (SCFA)-producing species such as Lactobacillus, Bifidobacterium, and Akkermansia, while simultaneously inhibiting pathogenic strains. These findings highlight the role of polyphenols in maintaining microbiome homeostasis and supporting epidermal barrier integrity. The review encompasses findings from clinical studies, animal models, and mechanistic investigations, while also addressing limitations related to polyphenol bioavailability. Overall, polyphenols may represent a valuable adjunctive approach in AD management; however, further well-designed clinical and mechanistic studies are required to confirm their therapeutic potential.},
}

Humans
*Polyphenols/pharmacology/therapeutic use
*Dermatitis, Atopic/drug therapy/microbiology/metabolism
Filaggrin Proteins
Animals
Gastrointestinal Microbiome/drug effects
*Anti-Inflammatory Agents/pharmacology
Inflammation/drug therapy
*Lipid Metabolism/drug effects
Epidermis/drug effects/metabolism
Signal Transduction/drug effects
*Microbiota/drug effects

@article {pmid42124000,
year = {2026},
author = {Schubert, MG and Dentand, A and Karczewski, M and Morsy, Y and Beuschlein, F and Scharl, M and Krayenbuehl, PA},
title = {Dose-Dependent Alterations of the Human Gut Microbiome During Oral Iron Supplementation: A Randomized Study in Iron-Deficient Non-Anaemic Women.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42124000},
issn = {2072-6643},
mesh = {Humans ; Female ; *Gastrointestinal Microbiome/drug effects ; Adult ; *Dietary Supplements ; *Iron/administration & dosage/adverse effects ; Administration, Oral ; Dose-Response Relationship, Drug ; Feces/microbiology ; Young Adult ; RNA, Ribosomal, 16S/genetics ; Iron Deficiencies ; },
abstract = {Background/Objectives: Oral iron supplementation is widely used to treat iron deficiency but frequently causes gastro-intestinal side effects that limit treatment adherence. Unabsorbed luminal iron has been proposed to influence intestinal microbial communities, yet the effects of different oral iron doses on the human gut microbiome remain insufficiently characterized. Methods: In this randomized open-label study, 30 healthy premenopausal women with iron deficiency without anaemia received either low-dose oral iron supplementation (6 mg twice daily) administered under fasting conditions or standard-dose iron supplementation (100 mg once daily) taken with a meal for four weeks. Stool samples were collected before and after treatment and analyzed using 16S rRNA sequencing to evaluate microbiome composition. Results: Baseline characteristics, including age, body mass index, hemoglobin concentration and serum ferritin, were comparable between groups. After four weeks of treatment, distinct alterations in gut microbiome composition were observed between the low-dose and standard-dose groups. The genera Colidextribacter and GCA-900066575 decreased in the low-dose group but increased in the standard-dose group, whereas Oscillospira showed the opposite pattern. Gastrointestinal adverse events were reported by 87% of participants receiving standard-dose iron supplementation compared with 7% receiving low-dose iron supplementation (p < 0.0001). Conclusions: Oral iron supplementation induces dose-dependent changes in the intestinal microbiome and higher doses are associated with substantially increased gastrointestinal intolerance. These findings suggest that lower iron doses may reduce microbiome disruption and improve treatment tolerability.},
}

Humans
Female
*Gastrointestinal Microbiome/drug effects
Adult
*Dietary Supplements
*Iron/administration & dosage/adverse effects
Administration, Oral
Dose-Response Relationship, Drug
Feces/microbiology
Young Adult
RNA, Ribosomal, 16S/genetics
Iron Deficiencies

@article {pmid42124002,
year = {2026},
author = {Caserta, S and Martino, EA and Skafi, M and Vigna, E and Bruzzese, A and Amodio, N and Fiorillo, M and Lucia, E and D'Arrigo, G and Olivito, V and Labanca, C and Mendicino, F and Alvaro, ME and Tripepi, G and Morabito, F and Gentile, M},
title = {The Gut Microbiota in Hematologic Malignancies: Mechanisms, Clinical Associations, and Translational Opportunities.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42124002},
issn = {2072-6643},
mesh = {Humans ; *Hematologic Neoplasms/microbiology/therapy ; *Gastrointestinal Microbiome/physiology ; Animals ; Translational Research, Biomedical ; Dysbiosis ; },
abstract = {Hematologic malignancies arise and progress within a systemic ecosystem in which the gut microbiota is an increasingly recognized, partially modifiable component. Across acute leukemias, chronic lymphocytic leukemia, plasma cell disorders, lymphomas, and clonal myeloid neoplasms, human studies consistently report reduced microbial diversity, depletion of barrier-supportive, short-chain fatty acid-producing commensals, and enrichment of Gram-negative, pro-inflammatory, or hospital-adapted taxa. These alterations are associated with pre-leukemic clonal expansion, adverse genetic and immunological features, progression from precursor conditions, and inferior outcomes after chemotherapy, immunochemotherapy, chimeric antigen receptor T-cell therapy, and allogeneic hematopoietic stem cell transplantation. Mechanistic work in animal models and ex vivo systems demonstrates that microbiota-derived signals and metabolites-including Th17/IL-17-skewing consortia and the lipopolysaccharide intermediate ADP heptose sensed by the cytosolic receptor ALPK1-can actively modulate hematopoietic stem and progenitor cell fitness, inflammatory circuits, and malignant cell survival, supporting a causal role in disease biology. At the same time, major knowledge gaps remain because most human cohorts are small, single-center, and cross-sectional, frequently rely on 16S rRNA profiling, and are vulnerable to dietary, geographic, and treatment-related confounding. Within this context, three translational domains appear particularly promising: pharmaco-microbiomics, microbiome-informed risk stratification, and rational microbiota-targeted interventions, particularly diet-based strategies and antimicrobial stewardship. Here, we provide an integrated, disease-spanning synthesis of these data, emphasizing clonal hematopoiesis and myeloid neoplasms as emerging examples of microbiota-marrow crosstalk and outlining practical priorities for embedding microbiome science into future hematologic trials. Routine microbiome profiling or empiric microbiota-directed therapies cannot yet be recommended in everyday hematology practice, but integrating microbiome science into prospective therapeutic and transplant trials offers a realistic path to improved disease modeling, biomarker development, and rational adjunctive strategies to enhance outcomes for patients with hematologic malignancies.},
}

Humans
*Hematologic Neoplasms/microbiology/therapy
*Gastrointestinal Microbiome/physiology
Animals
Translational Research, Biomedical
Dysbiosis

@article {pmid42124012,
year = {2026},
author = {Zeng, Y and Ahmed, M and Zhang, H},
title = {Beyond Antioxidants: The Microbial Metabolic Landscape of Anthocyanins and Their Downstream Health Implications.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42124012},
issn = {2072-6643},
support = {20243BCC31009//Key Project of Jiangxi Provincial Key Research and Development Program/ ; 32560560//National Natural Science Foundation of China/ ; },
mesh = {*Anthocyanins/metabolism/pharmacokinetics ; *Gastrointestinal Microbiome/physiology ; Humans ; *Antioxidants/metabolism ; Biological Availability ; Hydroxybenzoates/metabolism ; Animals ; Signal Transduction ; },
abstract = {BACKGROUND/OBJECTIVES: Anthocyanins are dietary pigments associated with reduced risk of chronic diseases, yet their low systemic bioavailability challenges the traditional direct antioxidant hypothesis. This review aims to reconceptualize anthocyanin bioactivity by proposing the gut microbiome as a key mediator that biotransforms these compounds into bioactive metabolites responsible for systemic health effects.

METHODS: This review synthesizes evidence on the microbial metabolism of anthocyanins and includes a structured appraisal of the literature using an evidence evaluation framework analogous to GRADE, focusing on their transit to the colon, enzymatic biotransformation by gut microbiota, and resulting production of phenolic metabolites such as protocatechuic acid (PCA). It also examines the role of specific bacterial taxa (e.g., Bifidobacterium and Lactobacillus) in enhancing bioavailability and explores the downstream cellular pathways modulated by these metabolites.

RESULTS: Gut microbiota convert anthocyanins into smaller phenolic metabolites such as PCA, syringic acid, gallic acid, and other respective metabolites, which achieve plasma concentrations up to 100-fold higher than parent compounds and can cross the blood-brain barrier. These metabolites exert systemic effects by modulating key signaling pathways (NF-κB and Nrf2) and restoring redox homeostasis. Additionally, beneficial gut bacteria enhance anthocyanin bioavailability and support the production of short-chain fatty acids (SCFAs).

CONCLUSIONS: Systemic health benefits of anthocyanins are largely mediated by gut microbiota through the generation of bioactive metabolites. This microbiota-driven process redefines the mechanistic understanding of anthocyanin action and highlights the microbiome as a critical determinant of their efficacy in preventing cardiometabolic and neurodegenerative diseases.},
}

*Anthocyanins/metabolism/pharmacokinetics
*Gastrointestinal Microbiome/physiology
Humans
*Antioxidants/metabolism
Biological Availability
Hydroxybenzoates/metabolism
Animals
Signal Transduction

@article {pmid42124014,
year = {2026},
author = {Uțu, D and Nodiți-Cuc, AR and Kiș, AM and Popovici, RA and Pitic, DE and Trusculescu, LM and Marian, D and Nan, AG and Matin, AS and Cîmpian, DM and Bodo, CR and Enache, A and Olariu, I},
title = {Diet-Microbiome-Brain Axis and Mental Health: Biological Mechanisms and Nutritional Implications.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42124014},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Mental Health ; *Brain/physiology ; Animals ; *Diet ; *Mental Disorders/prevention & control ; Probiotics ; Prebiotics/administration & dosage ; Dysbiosis ; },
abstract = {BACKGROUND/OBJECTIVES: Diet is a primary and modifiable determinant of gut microbiota composition, diversity, and metabolic activity, thereby shaping microbial-derived metabolites, immune and inflammatory signalling, neuroendocrine regulation, and neural communication with the central nervous system. Western dietary patterns, characterised by high intake of ultra-processed foods, saturated fats, and low dietary fibre, are consistently associated with gut dysbiosis, impaired intestinal barrier function, chronic low-grade inflammation, and increased risk of depression, anxiety, cognitive impairment, and neurodegenerative disorders.

METHODS: This narrative review synthesises evidence from human observational studies, randomised controlled trials, animal models, and mechanistic investigations examining interactions among diet, gut microbiota, and mental health or neurobiological outcomes. Literature searches were conducted in PubMed, Scopus, and Web of Science for articles published up to December 2025.

RESULTS: The study highlights the therapeutic potential and limitations of dietary interventions, prebiotics, probiotics, and psychobiotics, and critically evaluates them. Also facilitates an improved understanding of diet-microbiome-brain interactions, which may help the development of personalised, nutrition-based strategies integrated into mental health prevention and clinical care.

CONCLUSIONS: These findings support diet-based, microbiome-informed strategies as scalable adjuncts in mental health prevention and care.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Mental Health
*Brain/physiology
Animals
*Diet
*Mental Disorders/prevention & control
Probiotics
Prebiotics/administration & dosage
Dysbiosis

@article {pmid42124034,
year = {2026},
author = {Kłosek, S and Szymczak-Paluch, M and Bernaś, A and Gawlak-Socka, S},
title = {Does Probiotic Intake Enhance the Efficacy of Oral Fungal Infection Treatment?.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42124034},
issn = {2072-6643},
support = {503/2-148-07/503-21-001//Medical University of Lodz/ ; },
mesh = {*Probiotics/therapeutic use/administration & dosage ; Humans ; *Candidiasis, Oral/microbiology/therapy/drug therapy ; Antifungal Agents/therapeutic use ; Mouth/microbiology ; Microbiota ; },
abstract = {Oral candidiasis (OC) is the most frequent fungal infection among users of dental prosthetic devices, immunocompromised patients, and those who underwent chemotherapy treatment and had a complication of long-term antibiotic therapy. About 150 species of Candida fungi have been described, whereas over 80% of oral fungal infections are attributed to the opportunistic pathogen Candida albicans. Pain, dryness of oral mucosa, pathological lesions, and intermittent mucosal bleeding are the main symptoms that worsen the daily functioning of the abovementioned fungal-infected patients. A promising adjunctive strategy may involve the use of probiotic bacteria to attenuate fungal colonization in the oral cavity in order to reduce the need for conventional treatment, which carries a risk of antifungal drug resistance-a significant problem worldwide. Probiotic formulations mostly incorporate commensal bacteria that naturally inhabit oral ecosystems such as Lactobacillus spp., Bifidobacterium spp., Bacillus spp., and others. Probiotic organisms may contribute to the restoration of oral microbiome homeostasis through numerous mechanisms, such as competitive control of Candida species numbers, better adhesion to oral mucosa and production of bioactive compounds and antimicrobial metabolites. Despite many studies, the current evidence base remains heterogeneous. Well-designed studies across diverse populations are required to determine whether probiotic-based interventions can be an effective and clinically useful alternative or adjunct to standard antifungal therapy of OC.},
}

*Probiotics/therapeutic use/administration & dosage
Humans
*Candidiasis, Oral/microbiology/therapy/drug therapy
Antifungal Agents/therapeutic use
Mouth/microbiology
Microbiota

@article {pmid42124041,
year = {2026},
author = {Son, JY and Do, Y and Seo, J and Choi, J},
title = {Gut-Derived Metabolic Imbalance in Autism Spectrum Disorder: Toward the Concept of a Metabolic Subtype.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42124041},
issn = {2072-6643},
support = {Ky-lin Foundation in 2024//Daegu Haany University/ ; },
mesh = {Humans ; *Autism Spectrum Disorder/metabolism/microbiology ; *Gastrointestinal Microbiome/physiology ; *Fatty Acids, Volatile/metabolism ; Dysbiosis/metabolism ; *Gastrointestinal Tract/metabolism ; Animals ; },
abstract = {Autism spectrum disorder (ASD) is highly heterogeneous in symptom onset and severity, comorbidities, and treatment responsiveness, challenging the notion of a single pathogenic mechanism. Increasing evidence indicates that some individuals with ASD exhibit prominent peripheral physiological alterations, including gastrointestinal (GI) dysfunction, gut microbial dysbiosis, immune imbalance, oxidative stress, and mitochondrial/energy metabolic vulnerability. In this context, gut-derived metabolites-particularly short-chain fatty acids (SCFAs)-have emerged as plausible modulators of the neurodevelopmental milieu through the expanded gut-immune-metabolic-brain axis. This review synthesizes: (i) SCFAs' biogenesis and physiological roles, (ii) context- and developmental stage-dependent effects, (iii) the clinical heterogeneity of reported microbiome and SCFA alterations in ASD, and (iv) propionate as a frequently discussed candidate signal and the interpretive boundaries of preclinical evidence. Human studies show substantial inter-study variability in SCFA alterations (increases, decreases, or no differences), influenced by factors such as sample type (stool vs. blood), GI symptoms, diet, medication exposure, and analytical variability. Accordingly, SCFAs should not be treated as universal ASD biomarkers but rather as context-dependent metabolic signals relevant under specific clinical and biological conditions. Building on this premise, we propose the conceptual framework of "metabolic ASD" representing a metabolically informed dimension of biological variability in which peripheral metabolic-immune perturbations may contribute to neurodevelopmental vulnerability. To avoid premature causal claims, we outline design requirements for future research, including stratified study designs, longitudinal cohorts, and integrative multi-layer analyses. Ultimately, metabolic ASD should be positioned as a testable precision medicine research framework rather than a universal etiological model.},
}

Humans
*Autism Spectrum Disorder/metabolism/microbiology
*Gastrointestinal Microbiome/physiology
*Fatty Acids, Volatile/metabolism
Dysbiosis/metabolism
*Gastrointestinal Tract/metabolism
Animals

@article {pmid42124048,
year = {2026},
author = {Thakur, D and Harmer, MJ},
title = {Circulating Short-Chain Fatty Acid Levels in Chronic Kidney Disease: A Systematic Review and Meta-Analysis.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42124048},
issn = {2072-6643},
mesh = {Humans ; *Fatty Acids, Volatile/blood ; *Renal Insufficiency, Chronic/blood ; Child ; Adult ; Butyrates/blood ; Female ; Male ; Propionates/blood ; },
abstract = {BACKGROUND: Chronic kidney disease (CKD) is characterised by a disrupted gut-kidney axis, wherein intestinal dysbiosis is associated with the accumulation of uraemic toxins and the potential depletion of beneficial short-chain fatty acids (SCFAs). Whilst acetate, propionate, and butyrate are known to modulate systemic inflammation and blood pressure, their precise circulating concentrations across different CKD stages and age groups remain poorly defined. This systematic review and meta-analysis aimed to quantify blood SCFA concentrations in CKD patients compared to healthy controls.

METHODS: We conducted a systematic search of Medline, EMBASE, and the Cochrane Library for clinical studies reporting blood SCFA concentrations in humans with CKD. Methodological quality was assessed using the NIH tool. Standardised mean differences (SMDs) were calculated for the quantitative meta-analysis, with subgroup analyses performed for age, CKD stage, and treatment modality (dialysis vs. transplantation).

RESULTS: Twenty-one studies encompassing 9661 participants were included. Quantitative synthesis revealed a significant and consistent systemic depletion of circulating acetate and propionate in adult CKD patients compared to healthy controls (p < 0.05). This depletion followed a stage-dependent trajectory, worsening alongside declining glomerular filtration rates. Notably, a "butyrate paradox" was identified in paediatric cohorts; whilst adults showed progressive butyrate depletion, children with CKD often maintained or exhibited elevated levels, particularly in the context of hypertension. Furthermore, whilst haemodialysis patients exhibited the most profound SCFA deficiencies, kidney transplantation appeared to partially restore these metabolites toward healthy baseline levels.

CONCLUSIONS: CKD is associated with a profound systemic reduction in acetate and propionate, supporting the model of a compromised gut-kidney axis based on converging evidence. The divergent results for butyrate in paediatric versus adult populations suggest that SCFA metabolism is influenced by age-related factors or compensatory mechanisms. These findings highlight the potential for SCFA monitoring as a candidate or emerging markers for detecting early renal damage and stratifying risk.},
}

Humans
*Fatty Acids, Volatile/blood
*Renal Insufficiency, Chronic/blood
Child
Adult
Butyrates/blood
Female
Male
Propionates/blood

@article {pmid42124049,
year = {2026},
author = {Liu, H and Shi, CY and Fahey, JW},
title = {Sulforaphane in Cutaneous Disorders and Skin Injury: Mechanisms, Evidence, and Clinical Perspectives.},
journal = {Nutrients},
volume = {18},
number = {9},
pages = {},
pmid = {42124049},
issn = {2072-6643},
mesh = {Humans ; *Isothiocyanates/pharmacology/therapeutic use ; Sulfoxides ; *Skin Diseases/drug therapy/metabolism ; Animals ; *Skin/drug effects/metabolism/injuries ; Signal Transduction/drug effects ; Anti-Inflammatory Agents/pharmacology ; Oxidative Stress/drug effects ; Antioxidants/pharmacology ; },
abstract = {Cutaneous disorders such as atopic dermatitis, psoriasis, acne vulgaris, and rosacea, together with UV-induced skin injury and photoaging, are highly prevalent conditions that involve varying contributions from dysregulated immune responses, cutaneous inflammation, oxidative stress, barrier dysfunction, microbiome alteration, and exogenous injury. However, these conditions are biologically heterogeneous and should not be regarded as a single mechanistic class. Sulforaphane, a naturally occurring isothiocyanate found primarily in broccoli and other cruciferous vegetables, has attracted interest in dermatology because of its antioxidant, cytoprotective, and context-dependent anti-inflammatory properties. Sulforaphane exerts its biological effects by modulating key signaling pathways, particularly the Keap1/Nrf2 pathway and, in some settings, NF-κB-related signaling, thereby reducing oxidative stress and inflammation, regulating immune responses, enhancing skin barrier function, and potentially influencing the cutaneous microbiome. Preclinical studies and limited human data suggest that sulforaphane may reduce erythema, edema, and other markers of cutaneous damage in selected settings. This comprehensive review explores the role of sulforaphane across heterogeneous cutaneous conditions, with emphasis on molecular mechanisms, disease-specific differences, current evidence, and discusses key translational constraints including formulation, delivery, lack of standardized dosing, and the limitations of cell culture and animal models for predicting human efficacy. Overall, sulforaphane should presently be regarded as a promising but still early-stage translational candidate in dermatology. Robust human efficacy data remain lacking for chronic inflammatory dermatoses such as psoriasis, atopic dermatitis, acne, and rosacea, whereas the strongest current human evidence relates to UV-associated skin outcomes and photoprotection.},
}

Humans
*Isothiocyanates/pharmacology/therapeutic use
Sulfoxides
*Skin Diseases/drug therapy/metabolism
Animals
*Skin/drug effects/metabolism/injuries
Signal Transduction/drug effects
Anti-Inflammatory Agents/pharmacology
Oxidative Stress/drug effects
Antioxidants/pharmacology

@article {pmid42124376,
year = {2026},
author = {Moltrasio, C and Marzano, AV and Romagnuolo, M},
title = {The Multifaceted Role of Keratinocytes in Hidradenitis Suppurativa Pathogenesis.},
journal = {Experimental dermatology},
volume = {35},
number = {5},
pages = {e70269},
pmid = {42124376},
issn = {1600-0625},
support = {//Italian Ministry of Health (Ricerca Corrente) of Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan (Italy)./ ; },
mesh = {Humans ; *Hidradenitis Suppurativa/immunology/etiology/physiopathology ; *Keratinocytes/physiology ; Cytokines/metabolism ; Signal Transduction ; Inflammation ; Animals ; },
abstract = {Hidradenitis suppurativa (HS) is a chronic autoinflammatory skin disorder of the pilosebaceous unit, with multiple factors contributing to its onset, activity and progression. Alongside a predisposing genetic background, hormonal and microbiome alterations, dysregulation of innate and adaptive immune response, as well as environmental/epigenetic factors contribute to its immunopathogenic landscape. In the past years, translational investigations identified several distinct inflammatory networks, not only in the chronic but also in the early stages of disease, making them potential therapeutic targets. Emerging evidence underlies the important role of keratinocytes in the pathogenesis and progression of HS, acting not only as targets of inflammatory signaling pathways but also as active producers of pro-inflammatory cytokines, chemokines and effector molecules that may influence disease onset and activity. Despite these insights, different aspects of their involvement remain underexplored, necessitating further targeted research. This review aims to highlight the experimental evidence supporting the crucial role of keratinocytes in the inflammatory response and overall pathophysiology of HS.},
}

Humans
*Hidradenitis Suppurativa/immunology/etiology/physiopathology
*Keratinocytes/physiology
Cytokines/metabolism
Signal Transduction
Inflammation
Animals

@article {pmid42124457,
year = {2026},
author = {Wang, C and Xu, Z and Ma, M and Fu, Z and Yao, K},
title = {Gallic Acid Protects Against DSS-Induced Colitis by Modulating Gut Microbiota and Suppressing the Activation of NF-κB/MAPK Signaling Pathway.},
journal = {Molecular nutrition & food research},
volume = {70},
number = {9},
pages = {e70487},
doi = {10.1002/mnfr.70487},
pmid = {42124457},
issn = {1613-4133},
support = {LY22B070007//Natural Science Foundation of Zhejiang Province/ ; },
mesh = {Animals ; *Gallic Acid/pharmacology ; *Gastrointestinal Microbiome/drug effects ; Humans ; *NF-kappa B/metabolism ; Mice, Inbred C57BL ; Caco-2 Cells ; Mice ; Dextran Sulfate/toxicity ; *MAP Kinase Signaling System/drug effects ; Male ; RAW 264.7 Cells ; *Colitis/chemically induced/prevention & control/drug therapy ; Cytokines/metabolism ; Colon/pathology/drug effects ; Coculture Techniques ; },
abstract = {To investigate the protective role and mechanisms of gallic acid (GA) against ulcerative colitis (UC), C57BL/6 mice were pretreated with GA (10 or 50 mg/kg) or saline for 21 days before colitis induction with 2.5% DSS for 7 days. An in vitro Caco-2/RAW 264.7 coculture model mimicking the intestinal epithelium was used. After 24-h GA pretreatment, inflammation was induced with LPS in Caco-2/RAW 264.7 coculture cell for 4 h. GA alleviated colitis symptoms, improving body weight, preventing colon shortening, reducing histopathological damage, and lowering pro-inflammatory cytokines (IL-6, IL-22, TNF-α, IL-17α). It enhanced intestinal barrier integrity by upregulating tight junction (TJ) proteins claudin-1 and occludin. Mechanistically, GA inhibited NF-κB and MAPK pathways by suppressing phosphorylation of p65, IκB, JNK, ERK, and P38 in colon tissue. GA also favorably modulated the gut microbiome, reducing pathobionts (e.g., Desulfovibrio) and enriching beneficial genera like Enterobacteria and Prevotella. In the cell coculture model, GA suppressed LPS-induced pro-inflammatory mediators, upregulated IL-10, and restored LPS-downregulated TJ protein expression. These findings indicate that GA alleviates DSS-induced UC by restoring intestinal homeostasis, exerting anti-inflammatory effects, and providing preventive benefits upon long-term use, supporting its potential as a prophylactic agent for UC.},
}

Animals
*Gallic Acid/pharmacology
*Gastrointestinal Microbiome/drug effects
Humans
*NF-kappa B/metabolism
Mice, Inbred C57BL
Caco-2 Cells
Mice
Dextran Sulfate/toxicity
*MAP Kinase Signaling System/drug effects
Male
RAW 264.7 Cells
*Colitis/chemically induced/prevention & control/drug therapy
Cytokines/metabolism
Colon/pathology/drug effects
Coculture Techniques

@article {pmid42124488,
year = {2026},
author = {Koynova-Tenchov, R},
title = {Molecular Dialogues in the Mitochondria-Microbiome Crosstalk: Metabolites, Signaling, and Immunity.},
journal = {Comprehensive Physiology},
volume = {16},
number = {3},
pages = {e70164},
doi = {10.1002/cph4.70164},
pmid = {42124488},
issn = {2040-4603},
mesh = {Humans ; *Mitochondria/metabolism ; Animals ; Signal Transduction/physiology ; *Microbiota/physiology ; *Gastrointestinal Microbiome/physiology ; },
abstract = {The bidirectional dialogue between mitochondria and the human microbiota-the mitochondria-microbiome axis-plays a pivotal role in regulating host metabolism, immune signaling, and overall physiological homeostasis. Growing evidence underscores the role of microbial metabolites-including short-chain fatty acids, secondary bile acids, and lipopolysaccharides-as direct modulators of mitochondrial bioenergetics, redox balance, and inflammatory cascades. Conversely, mitochondrial integrity governs the microbial landscape by regulating local oxygen tension, modulating immune-mediated selection, and secreting metabolic byproducts that shape commensal populations. Disruptions to this bidirectional crosstalk are linked to a diverse pathological spectrum. These include metabolic syndromes like obesity, type 2 diabetes, and NAFLD; neurodegenerative disorders such as Parkinson's and Alzheimer's; and systemic inflammatory conditions, notably inflammatory bowel disease and various autoimmune pathologies. Therapeutic interventions designed to modulate this axis-ranging from targeted probiotics, dietary interventions, and mitochondrial boosters-offer significant potential for reinstating physiological homeostasis. This review explores the molecular foundations of mitochondria-microbiome crosstalk, its role in disease pathogenesis, and the potential for microbiome-targeted therapies to restore mitochondrial health. Unraveling this complex dialogue may open new avenues for treating diseases rooted in metabolic and microbial dysbiosis. On the basis of a wide-ranging literature survey, the frontiers of the molecular dialogues involved in the mitochondria-microbiome communications are evaluated. By analyzing publication trends, we identify nascent perspectives and transformative concepts, mapping the mitochondria-microbiome axis research, aiming to bridge the gap between basic science and translational applications. This synthesis offers a fresh lens for treating diseases rooted in this intricate biological interplay.},
}

Humans
*Mitochondria/metabolism
Animals
Signal Transduction/physiology
*Microbiota/physiology
*Gastrointestinal Microbiome/physiology

@article {pmid42124590,
year = {2026},
author = {Schell, LD and Liow, YJ and Carmody, RN},
title = {Fasting and re-feeding independently alter mouse gut microbiota during intermittent fasting.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.25.707984},
pmid = {42124590},
issn = {2692-8205},
abstract = {Intermittent fasting (IF) elicits metabolic benefits that are partially driven by the gut microbiome. Studies have focused on endpoint IF-induced changes in the gut microbiome but have not explored whether the oscillating nature of IF elicits day-to-day microbiome changes that could independently affect health. To discriminate the long-term and short-term effects of IF on the gut microbiota, we fasted mice every other day (IF1:1) or every two days (IF1:2), measuring daily changes in body mass and composition, food intake, and gut microbiota composition. We show that short-term effects of fasting and re-feeding on gut microbiota composition outweigh longer-term effects of IF treatment, with composition responding differently to re-feeding and fasting. Re-feeding specifically promoted rapid expansion of Lactobacillus , a bacterial genus linked mechanistically to the metabolic benefits of IF. Our results highlight the plasticity of the gut microbiota, especially re-feeding effects, as a potential contributor to microbiome-mediated metabolic benefits of IF.},
}

@article {pmid42124632,
year = {2026},
author = {Adade, EE and Wang, R and Henneberry, CM and Lemus, AA and Stevick, RJ and Perez-Pascual, D and Audrain, B and Orsino, AJ and Farnsworth, DR and Ghigo, JM and Valm, AM},
title = {Cross hybridization Inference for Phylogenetic Resolution (CIPHR)-FISH enables microbiome imaging with strain level taxonomic resolution.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.26.708344},
pmid = {42124632},
issn = {2692-8205},
abstract = {The spatial organization of microbial communities is a critical determinant of host-microbe interactions, yet species-level mapping remains challenging due to high 16S rRNA sequence homology and spectral crosstalk in multiplexed fluorescence in situ hybridization (FISH). To address this challenge, we developed Cross-hybridization Inference for Phylogenetic Resolution (CIPHR)-FISH, a pipeline that integrates strategic probe design with supervised machine learning. CIPHR-FISH transforms probe cross-hybridization and spectral overlap, traditionally viewed as experimental noise, into informative molecular signatures. Using a gnotobiotic zebrafish model colonized with a defined mix of 10 zebrafish bacterial strains, we trained a support vector machine (SVM) on empirical hybridization patterns from pure bacterial cultures. CIPHR-FISH achieved 99.2 % macro-averaged accuracy, significantly outperforming standard linear unmixing (62.5 %), and successfully discriminated strains with 99.7% sequence homology. Applying this tool to gnotobiotic zebrafish larvae revealed distinct biogeographies: the intestinal bulb hosted highly structured, multi-layered polymicrobial aggregates, while the skin exhibited sparse, uniformly dispersed individual bacterial cells. Notably, we observed significant inter-individual variation in spatial community structure that was obscured by traditional bulk 16S rRNA sequencing. CIPHR-FISH provides a robust, scalable framework for high-resolution spatial biology by converting the limitations of molecular labeling into a rich data source for taxonomic classification. This approach enables the quantification of micro-scale ecological and stochastic forces that shape the microbiome across hosts.},
}

@article {pmid42124675,
year = {2026},
author = {Badenoch, AJ and Pang, Z and Chung, CH and Robida, A and Badenoch, B and Natesan, R and Kakish, L and Li, J and Chandrasekaran, S},
title = {Modeling Microbiome Modulation of Tumor Metabolic Networks to Predict Synergistic Therapies.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.25.707963},
pmid = {42124675},
issn = {2692-8205},
abstract = {Differences in microbiome composition profoundly influence drug response, yet methods to model the metabolic interplay between tumors, microbes, and therapeutics remain limited. We present a generalizable framework combining machine-learning and genome-scale metabolic modeling to prioritize combination therapies for colorectal cancer (CRC) in the presence of Fusobacterium nucleatum (Fn) and other pathogenic, probiotic, and commensal microbes. Trained on 6,514 drug combinations in microbe-free CRC cell lines, the model predicted synergistic combinations in both microbe-free and microbe-associated contexts and generalized to immunotherapy-associated conditions. Predictions were validated using an asymmetric co-culture system that mimics the colon's normoxic-anaerobic gradient, confirming synergistic combinations in HCT116 cells with Fn , including drugs not typically used in CRC therapy. Mechanistic analysis and targeted pharmacological perturbations revealed phospho-inositol metabolism and cysteine transport as key determinants of Fn -dependent drug synergy. Together, this work introduces a scalable, microbiome-aware framework to enable discovery of context-specific combination therapies.},
}