@article {pmid41907525,
year = {2026},
author = {González-Valdivia, C and Tong, B and Hjalmarsson, S and Guðnadóttir, U and Wagner, N and Engstrand, L and Schuppe-Koistinen, I and Fransson, E and Prast-Nielsen, S and Brusselaers, N and Hugerth, LW},
title = {The gut microbiome in early pregnancy is associated with the severity of nausea and vomiting: a nested case‒control study.},
journal = {Gut microbes reports},
volume = {3},
number = {1},
pages = {2603861},
pmid = {41907525},
issn = {2993-3935},
abstract = {Approximately 70% of all pregnancies are affected by nausea and vomiting (NVP), yet the mechanisms controlling this phenomenon are not well known. Pregnancy hormones explain a large part of this effect, mostly through human chorionic gonadotropin and fetal production of GDF15, a hormone active in the brain stem. Still, there is a wide variation in the severity of symptoms, ranging from no nausea to severe vomiting requiring hospitalization (hyperemesis gravidarum). Here, we present a nested case‒control study within the large SweMaMi cohort, wherein 337 participants with severe NVP in early pregnancy were matched 1-to-1 with moderate and mild NVP, respectively. Subjects with more severe nausea had lower richness and diversity in their fecal microbiomes. Several taxa were significantly associated with NVP score, where the most extreme are a negative correlation with Lactobacillaceae and positive correlations with Bifidobacterium dentium and Puniceicoccaceae. Finally, higher NVP score was associated with a higher abundance of bacteria encoding for the neuroactive pathways of glutamine degradation, inositol synthesis, and lactate production. In conclusion, the gut microbiota was strongly associated with NVP. Further studies with direct interventions capable of restoring the early-pregnancy gut microbiome could open up new approaches for dealing with the most common symptom of early pregnancy.},
}

@article {pmid41907632,
year = {2026},
author = {Russo, F and Tripodi, L and Caldora, F and Pandolfo, SD and Aveta, A and Nardelli, C and Imbimbo, C and Perdonà, S and Pastore, L and Castaldo, G},
title = {Identification of a weighted urinary microbial signature for bladder cancer discrimination.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1784501},
pmid = {41907632},
issn = {2234-943X},
abstract = {INTRODUCTION: Growing evidence from microbiome studies has demonstrated associations between dysbiosis and cancers, including bladder cancer (BCa). Our recent works on urobiome revealed a different microbial composition in BCa patients compared to controls. The aim of this work was to create a Weighted Composite Index (WCI) to distinguish BCa-affected patients (mBCa) from healthy controls (mHC) in a cohort of male aged over 50 years.

METHODS: Urobiome data from 51 subjects (27 mBCa and 24 mHC) were analyzed. Random Forest (RF) classifier was trained to identify genera and species which significantly contributed to discriminating between mBCa and mHC group. A weighted normalization approach was used to compute separate WCIs at genus and species levels and in-silico validation test were performed to assess the models' robustness.

RESULTS: the WCI was calculated for each patient at both genera and species levels, showing a significant difference between the two groups (p < 0.0001) in both comparisons. WCIs showed superior discriminative performances compared to any individual taxon used for the model construction. Despite the need for validation in larger independent cohorts, the in-silico validation pipeline showed a stable high sensitivity of the models.

CONCLUSIONS: Our findings identified a candidate urinary microbial signature in a biomarker discovery setting associated with bladder cancer. This hypothesis-generating approach may contribute to the identification of a non-invasive biomarker, which requires validation in larger, independent cohorts before clinical application.},
}

@article {pmid41907707,
year = {2024},
author = {Teigen, LM and Kaiser-Powers, T and Matson, M and Elkin, B and Kabage, AJ and Hamilton, M and Vaughn, BP and Sadowsky, MJ and Staley, C and Khoruts, A},
title = {Contribution of Common Sulfur-Containing Substrates to Hydrogen Sulfide Production By Human Gut Microbiota Using an In Vitro Model Standardized For Bacterial Counts.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {2361246},
pmid = {41907707},
issn = {2993-3935},
abstract = {Hydrogen sulfide (H2S) produced by human gut microbiota is highly toxic and implicated in pathogenesis of gastrointestinal tract disorders. Sulfur-containing amino acid (SAA) degradation is a major contributor to its production, but SAA degradation pathways have not been extensively characterized. In vitro model systems of fecal H2S production offer a basic method to help elucidate SAA degradation pathways, but the approach is not standardized. To address this, we used fecal microbiota separated from feces and standardized for bacterial counts to measure H2S production potential in response to different substrates in healthy controls (n = 6) with repeated sampling (three samples per participant). H2S production was highest with cysteine (mean = 16.7 ppm) compared to sodium sulfate (0.7 ppm) and taurine (0.8 ppm). Sodium-sulfate-driven H2S production negatively correlated with Ruminococcus (Spearman's ρ = -0.5) and cysteine-driven H2S production negatively correlated with Firmicutes (Spearman's ρ = -0.5). These findings, using a protocol controlling for confounding variables such as bacterial counts, validate previous findings of cysteine as a primary driver of H2S production. Finally, the inclusion of samples from two patients with UC allowed for the illustration of the potential of this approach to identify functional differences in specific disease states.},
}

@article {pmid41907708,
year = {2024},
author = {Kaufman, P and O'Meara, KE and Hawrelak, J},
title = {Preventing chemotherapy-induced diarrhea and microbiota imbalances with prebiotics and probiotics in breast cancer treatment: A case report.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {2379475},
pmid = {41907708},
issn = {2993-3935},
abstract = {Breast cancer (BC) is the second most common cancer in women in the United States. Of those diagnosed, 40-80% will undergo chemotherapy. Adverse effects of chemotherapy are chemotherapy-induced diarrhea (CID) and gut microbiota dysregulation. CID can lead to dehydration, metabolic acidosis, malnutrition, and gut dysbiosis. Antidiarrheal medications are the standard treatment of care; however, this has been shown to further contribute to gut dysbiosis, is not always effective in controlling diarrhea, and can lead to rebound constipation with the potential of pathogenic bacterial overgrowth. In this case report, we describe the experience of a patient-centered, personalized intervention with pre- and probiotics to preserve the microbiota and prevent CID. A 57-year-old postmenopausal female with BC undergoing adriamycin-cyclophosphamide (AC) and taxol-cyclophosphamide (TC) chemotherapies for invasive ductal carcinoma under the care of a cancer team wanted to refrain from using loperamide and instead use nutritional interventions and supplementation for preventing CID and maintaining gut health. This case report is a narrative report of the observed outcomes of one patient with BC after taking specific prebiotics and probiotics. The outcomes included the prevention of CID and other gastrointestinal adverse effects, and maintaining microbiota alpha-diversity, butyrate producing genera, and Bifidobacterium populations while inhibiting the overgrowth of Proteobacteria pathogenic bacteria.},
}

@article {pmid41907711,
year = {2024},
author = {Varshney, N and Pandey, RK and Mishra, A and Kumar, S and Jha, HC},
title = {Aurora Kinase A: Integrating Insights into Cancer, Inflammation, and Infectious Diseases.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {2419069},
pmid = {41907711},
issn = {2993-3935},
abstract = {Aurora kinase A (AURKA) is crucial in regulating cell division and maintaining genomic stability, making it significant in cancer biology. This review explores AURKA's structural and functional roles, emphasizing its involvement in cell cycle progression. Beyond cancer, AURKA emerges as a multifaceted player in host cell modulation, exerting influence over inflammatory responses, cell death mechanisms, and autophagy pathways. Moreover, recent research highlights its involvement in viral and bacterial infections. Numerous viruses, for their replication and assembly, modulate host cell cycle progression. Various viruses modulated AURKA to induce viral-mediated tumor. It also emerged as a key modulator in various gut microbiome-mediated cancers. Further, it also imparts oncogenic effect by modulation in cytoplasmic and mitochondrial regions of the cell. It hampers DNA replication independent of its kinase domain. Understanding AURKA's diverse roles underscores its potential as a promising drug target, offering therapeutic avenues for various diseases. This comprehensive exploration navigates through complex landscape of AURKA biology, paving way for future investigations and therapeutic interventions.},
}

@article {pmid41907714,
year = {2024},
author = {Molinas-Vera, M and Ferreira-Sanabria, G and Peña, P and Sandoval-Espinola, WJ},
title = {The Paraguayan gut microbiome contains high abundance of the phylum Actinobacteriota and reveals the influence of health and lifestyle factors.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {2332988},
pmid = {41907714},
issn = {2993-3935},
abstract = {Most gut microbiome studies are focused on populations from developed nations. However, this overlooks the role played by host genetics, lifestyle, and diet, highlighting the need to evaluate under-represented populations. Thus, we performed the first gut microbiome study from a Paraguayan cohort via 16S rRNA sequencing and PICRUSt2 analysis. We evaluated fecal samples from 60 participants from Asunción, while considering categories such as body-mass-index (BMI), sex, age, diet, lifestyle, and clinical history. Firmicutes (76.0 ± 11.6%), Actinobacteriota (10.4 ± 7.9%) and Bacteroidota (9.4 ± 11.4%) were the most abundant phyla. Similarly, the most abundant genera were Blautia (14.1 ± 7.5%), Faecalibacterium (8.07 ± 6.8%), and Bacteroides (6.7 ± 6.8%). Likewise, the most abundant microbial pathways were predicted to be involved with sugar metabolism and fermentation. Interestingly, some categories significantly impacted the gut microbiome composition and function, such as BMI (Moryella, Bifidobacterium), sex (Faecalibacterium), and others. Additionally, dysbiotic indices differed from values previously reported as homeostatic. These observations highlight the need for further studies, considering microbial species and host genetics. Thus, this work expands the knowledge of the gut microbiome from the Collective South, while contrasts found herein reinforce the need for further research with human populations traditionally understudied.},
}

@article {pmid41907715,
year = {2024},
author = {Winters, AD and Francescutti, DM and Kracht, DJ and Kuhn, DM and Angoa-Perez, M},
title = {The Effects of Ceftriaxone on Glutamate Transporter Expression and the Gut Microbiome: Implications for a Role of Antibiotic-Induced Dysbiosis in Mediating Drug Seeking and Relapse.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {2393727},
pmid = {41907715},
issn = {2993-3935},
abstract = {Ceftriaxone (CTX), a beta-lactam antibiotic, is widely used in drug seeking and relapse studies due to its ability to enhance glutamate transporter (GLT-1) expression in the brain. Since increased synaptic glutamate is believed to drive drug seeking and relapse, CTX's effect on GLT-1 offers potential for treating substance abuse. However, the effect of CTX on the gut microbiome remains unexplored. Mice received CTX at 200 mg/kg per day for 4 d, and its effects on the gut microbiome were assessed. CTX led to increased striatal GLT-1 expression and induced rapid, long-lasting dysbiosis, with females showing a greater response than males. Diversity metrics were significantly altered during the acute phase of CTX treatment. Alpha diversity showed varying recovery levels depending on sex, while beta diversity indicated that CTX-treated mice remained significantly different from controls. CTX caused significant increases in Bacillota and reductions in Bacteroidota. Most taxa were rapidly reduced by CTX, but Enterococcus and Bacillales expanded significantly. Metabolomic analysis revealed significant changes in microbial pathways related to substance use disorders. These findings indicate that CTX causes immediate and persistent alterations in the gut microbiome, highlighting the importance of considering the gut microbiome as a target in substance abuse treatment.},
}

@article {pmid41907718,
year = {2024},
author = {Tannock, GW},
title = {Scoring Microbiota Function: A Proposal to Use Features of Evolutionary, Symbiotic Innovation to Recognize a "Healthy" Human Gut Microbiota.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {2376543},
pmid = {41907718},
issn = {2993-3935},
abstract = {Research concerning the significance of the bacterial community of the human colon (gut microbiota or microbiome) in the etiology of diseases has depended in large part on molecular and bioinformatic tools to assemble catalogs of bacterial diversity. This article proposes that the gut microbiotas of humans are collectively a metacommunity whose functions are characteristic and consistent across all healthy humans. The pathway of evolutionary innovation in the development of the symbiosis between humans and gut microbiotas is known. Therefore, it is suggested that functional scoring of these long-lasting symbiotic innovations will reap greater benefits in delineating health or disease than can comparative taxonomic analysis. Adoption of a function-scoring approach would offer opportunities for emerging researchers, worldwide, to form multidisciplinary teams to develop essential methodologies to advance this gut microbiota research.},
}

@article {pmid41907719,
year = {2024},
author = {Dixit, K and Ahmed, A and Singh, A and Inamdar, M and Chavan, S and Bodkhe, R and Mehtab, W and Chauhan, A and Saroj, SD and Ahuja, V and Shouche, Y and Dhotre, D and Makharia, G},
title = {Site-Specific Gut Microbial Signatures in Non-Celiac Gluten Sensitivity.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {2438621},
pmid = {41907719},
issn = {2993-3935},
abstract = {Gut microbiota in non-celiac gluten sensitivity (NCGS) has been poorly studied for its involvement in the disorder and site specificity. We investigated small intestinal, large intestinal and stool microbiota profiles in patients with NCGS and highly overlapping disorder irritable bowel syndrome (IBS) as well as effect of gluten-free diet (GFD) on microbiota in patients with NCGS. True NCGS patients were recruited based on serological response for anti-gliadin antibodies, 6-week gluten free diet (GFD) and symptom recurrence with gluten-rechallenge. Analyses using 16S rRNA gene amplicon and shotgun sequencing revealed community differences in core microbiome and diversity measures across sample types indicating dysbiosis mainly in mucosa-associated small intestinal microbiome of NCGS patients. Genera Elusimicrobiaum, Succinivibrio, Bacillus and Alcaligenes appeared as signatures in small intestine and stool in NCGS patients. Presence of differential taxa co-occurring at sampling sites, enabled recognition of site-specific microbial signatures. GFD led to a shift in mucosa-associated small intestinal core microbiome. Metagenome analysis revealed subtle differences in pathways for amino acid biosynthesis including L-ornithine. Mucosa-associated small intestine microbial structure was quite distinct in patients with NCGS in comparison to that with IBS.},
}

@article {pmid41907720,
year = {2024},
author = {Funahashi, K and Lee, CG and Sugitate, K and Kagata, N and Fukuda, N and Song, I and Ishii, C and Hirayama, A and Fukuda, S},
title = {Development of a Specialized Method for Simultaneous Quantification of Functional Intestinal Metabolites by GC/MS-Based Metabolomics.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {2429408},
pmid = {41907720},
issn = {2993-3935},
abstract = {Intestinal metabolites produced by gut microbes play a significant role in host health. Due to their different chemical structures, they are often analyzed using multiple analyzers and methods, such as gas chromatography/mass spectrometry (GC/MS) for SCFAs and liquid chromatography/mass spectrometry (LC/MS) for bile acids (BAs), amino acids (AAs), and sugars. In this study, we aimed to develop a specialized method for the simultaneous determination of important intestinal metabolites, specifically addressing the main issue of SCFA volatilization during the dry solidification process. We discovered that these compounds can all be measured in fecal samples by GC/MS after trimethylsilyl (TMS) derivatization despite the expected volatility of SCFAs. Validating the results using SCFA standards suggested that the fecal matrix exerts a stabilizing effect. This method enabled the simultaneous quantification of 65 metabolites. For further validation in a biological context, a mouse study showed that high-MAC and high-fat diets increased SCFAs and BAs in feces, respectively, and showed a negative correlation between Alistipes and sugars, all consistent with previous studies. As a result, we successfully developed a specialized simultaneous quantification method for SCFAs, BAs, AAs, AA derivatives, and sugars in fecal samples using GC/MS-based metabolomics in conjunction with a TMS derivatization pretreatment process.},
}

@article {pmid41907847,
year = {2026},
author = {Tng, TJW and Vanan, S and Tan, EK and Zeng, L and Goh, WWB and Wong, SH and Lim, KL},
title = {Examination of shared gut microbiome signatures in aging and Parkinson's disease.},
journal = {Frontiers in aging neuroscience},
volume = {18},
number = {},
pages = {1745455},
pmid = {41907847},
issn = {1663-4365},
abstract = {Parkinson's disease (PD) is a prevalent neurodegenerative disorder that is characterized clinically by a constellation of motoric deficits including resting tremors, bradykinesia, and rigidity. In recent years, there has been increasing interest in the gut-brain axis with several studies examining the relationship between gut microbiome and PD. Although association studies have reported multidimensional microbiome changes in PD, these observed changes may be confounded by various factors, especially age. Notably, existing literature on gut microbiome tends to consider aging and PD separately. This review thus examines the gut microbiome factors associated with both aging and PD. Our comprehensive analysis of the available literature reveals significant overlaps in gut microbes that are associated with aging and PD. For example, the bacterial genera Akkermansia, and Alistipes have shown increased abundance in both conditions, while Faecalibacterium and Blautia conversely show decreased abundance. Our findings were temporally consistent with more recent studies. These shared gut microbiome signatures were identified in patients across the clinical spectrum of PD symptom severity, and may influence aging and disease pathogenesis via depletion of butyrate, a beneficial anti-inflammatory microbial metabolite, since major producers of butyrate (such as Faecalibacterium and Blautia) were constantly decreased with age (across both Asian and Western populations). Given these observations, we wish to highlight the need to consider age-related factors in understanding microbiome changes in PD; the intersection of which could reveal gut microbes and their corresponding microbial metabolites such as butyrate as potential therapeutic targets for PD.},
}

@article {pmid41907858,
year = {2026},
author = {Hashim, NT and Babiker, R and Padmanabhan, V and Islam, MS and Priya, SP and Chaitanya, NCSK and Mohammed, R and Dasnadi, SP and Ahmed, A and Gismalla, BG and Rahman, MM},
title = {Oral and cardiometabolic health through the lens of biobanks and large-scale epidemiologic research.},
journal = {Frontiers in oral health},
volume = {7},
number = {},
pages = {1774868},
pmid = {41907858},
issn = {2673-4842},
abstract = {Oral diseases and cardiometabolic disorders are among the most prevalent non-communicable conditions worldwide and share common inflammatory, metabolic, and social determinants. Over the past two decades, growing evidence has linked poor oral health-particularly periodontitis and tooth loss-to cardiometabolic outcomes such as type 2 diabetes and cardiovascular disease. However, progress in this field has long been constrained by fragmented data systems and limited availability of large-scale resources capturing both oral health exposures and cardiometabolic endpoints. Recent advances in biobank infrastructure, population-based cohorts, and electronic health record linkage have transformed this landscape, enabling robust secondary analyses at unprecedented scale. This narrative review synthesizes current evidence from major biobanks and large-scale epidemiologic datasets relevant to oral-cardiometabolic research. We describe how oral health and cardiometabolic outcomes are operationalized across data ecosystems, critically appraise the strengths and limitations of key resources, and integrate epidemiologic findings with established biological mechanisms, including chronic systemic inflammation, microbial dysbiosis, metabolic dysfunction, and vascular impairment. We further highlight the bidirectional nature of the relationship, whereby cardiometabolic disease can also exacerbate oral inflammatory conditions. Methodological challenges-such as exposure misclassification, residual confounding, and reverse causation-are discussed alongside emerging solutions, including data linkage, multi-omics integration, and advanced analytic approaches. Harnessing large-scale data sources offers a powerful opportunity to reposition oral health within cardiometabolic disease research and prevention. Strategic integration of dental and medical data has the potential to inform precision public health approaches and support more holistic models of chronic disease prevention.},
}

@article {pmid41907864,
year = {2026},
author = {Taudte, N and Liebe, L and Jänckel, N and Ramsbeck, D and Schilling, S and Potempa, J and Eick, S and Buchholz, M},
title = {Novel small molecule targeting PgQC reduces Porphyromonas gingivalis virulence.},
journal = {Frontiers in oral health},
volume = {7},
number = {},
pages = {1716188},
pmid = {41907864},
issn = {2673-4842},
abstract = {INTRODUCTION: Periodontitis, a chronic inflammatory disease affecting the periodontium, is primarily driven by dysbiosis of the oral microbiome with Porphyromonas gingivalis as a keystone pathogen. Current therapeutic approaches rely on mechanical debridement and antimicrobials, which face limitations including antibiotic resistance and microbiome disruption. Pathoblockers represent a novel therapeutic strategy that selectively targets virulence factors without bactericidal effects, potentially reducing resistance development while preserving beneficial microbiota. Here, we describe the characterization of S-0636, a novel reversible inhibitor of zinc-dependent glutaminyl cyclase (PgQC), as a compound to selectively inhibit the bacterial virulence of P. gingivalis.

METHODS: The compound's effects were assessed through enzymatic assays, bacterial growth studies, virulence factor activity measurements (gingipain activity, hemagglutination, keratinocyte invasion), selectivity testing against commensal oral bacteria, resistance development analysis over 50 passages, and cytotoxicity evaluation in human cell lines.

RESULTS: S-0636 demonstrated potent PgQC inhibition with a Ki value of 0.014 μM and has successfully reduced the intracellular PgQC activity by 50% at 8 μM and had no bactericidal effects. Treatment of P. gingivalis with S-0636 significantly decreased gingipain activity, impaired hemagglutination capacity, and reduced keratinocyte invasion by 76% at 62.5 μM. The compound showed high selectivity, with no growth inhibition of ten tested oral commensal species at concentrations up to 0.25 mM. Importantly, no resistance development was observed after 50 bacterial passages, and cytotoxicity remained minimal in human cell lines with >80% viability at 0.5 mM.

DISCUSSION: In previous studies, PgQC was suggested as an enzyme responsible for pGlu-modification and stabilization of bacterial virulence factors. The current study now validates PgQC as an attractive target for pathoblocker development, demonstrating that S-0636 effectively attenuates P. gingivalis pathogenicity through selective virulence factor inhibition while preserving bacterial viability and oral microbiome integrity. The absence of resistance development and low cytotoxicity profile support the potential clinical translation of this approach for periodontal disease management, representing a promising alternative to conventional antimicrobial therapies.},
}

@article {pmid41908157,
year = {2024},
author = {Pfavayi, LT and Sibanda, EN and Baker, S and Woolhouse, M and Mduluza, T and Mutapi, F},
title = {Diversity and composition of gut protist in young rural Zimbabwean children.},
journal = {Frontiers in microbiomes},
volume = {3},
number = {},
pages = {1399160},
pmid = {41908157},
issn = {2813-4338},
abstract = {BACKGROUND: The human gut microbiome harbours diverse species of archaea, bacteria, fungi, protists and viruses. To date, most gut microbiome studies have focused on bacteria, neglecting other microbial communities. Consequently, less is known about the diversity and abundance of the latter. Here, we aimed to characterise the diversity and composition of protists in the gut of preschool-aged children (PSAC) in rural Zimbabwe relative to host age, sex, and schistosome infection status.

METHODS: The gut protist of 113 PSAC (1-5 years) was examined via shotgun metagenomic sequencing and analysed for diversity. Variation in protist abundance with host and environmental factors was analysed by permutational multivariate analysis of variance (PERMANOVA). To investigate how the composition of specific taxa varies across age, sex, nutritional measures and Schistosoma hematobium infection status, analysis of the composition of microbiomes (ANCOM) was used.

RESULTS: Eighty protist genera were identified, and the most abundant genera detected was Blastocystis. The prevalence of pathogenic protists was comparatively low, with 12.4% and 3.4% of the participants' gut colonised by E. histolytica and Cryptosporidium, respectively. Of all the independent variables only S. haematobium infection showed significant relationship with the structure of the gut protist, being associated with increases in Peronospora, Pseudoperonospora, Plasmopara and Blastocystis (FDR= 0.009).

SUMMARY: This study provides data on the prevalence and diversity of the gut protists in young Zimbabwean children with an emphasis on the host factors; age, sex and schistosome infection status. Our results showed no association between the host factors investigated, including anthropometric measures adjusted for age and the intestinal protist composition and structure, but S. haematobium infection status was associated with composition of specific taxa. There is a need for more studies determining how pathogenic protist interact with non-pathogenic protist in people exhibiting clinical symptoms to inform therapy and nutraceuticals.},
}

@article {pmid41908202,
year = {2026},
author = {Awashra, A and Neiroukh, H and AbuBaha, M and Shehadeh, W and Jallad, H and Emara, A and Abu-Khazneh, O and Zahran, A and Elgendy, MS and Fkheideh, T and Sawaftah, Z and Milhem, F and Hajjeh, O and Shubietah, A},
title = {The gut-heart axis in atrial fibrillation: Pathophysiology, evidence, and therapeutic potential.},
journal = {Heart rhythm O2},
volume = {7},
number = {3},
pages = {581-597},
pmid = {41908202},
issn = {2666-5018},
abstract = {BACKGROUND: Recent advances in microbiome research highlight a bidirectional relationship between gut microbiota and atrial fibrillation (AF), the most common sustained arrhythmia worldwide. Gut dysbiosis has been implicated in systemic inflammation, metabolite imbalance, bile acid signaling, and autonomic dysfunction, whereas AF itself alters microbial homeostasis through hemodynamic and neurohormonal changes.

OBJECTIVE: This review aimed to synthesize current evidence linking gut dysbiosis to AF pathogenesis, identify mechanisms underlying this interaction, and explore the therapeutic potential of microbiota-targeted interventions.

METHODS: We conducted a narrative review of preclinical, clinical, and epidemiologic studies examining the gut-heart axis in AF. Particular emphasis was placed on microbial metabolites (eg, trimethylamine N-oxide, short-chain fatty acids, indoxyl sulfate), bile acid modulation, and inflammatory signaling. Data on interventions, including diet, probiotics, pharmacologic approaches, and fecal microbiota transplantation, were integrated to assess translational potential.

RESULTS: Evidence suggests that gut-derived signals contribute to atrial remodeling through activation of the NLRP3 inflammasome, altered calcium handling, and impaired gap junction integrity. Conversely, AF promotes dysbiosis by reducing gut perfusion, altering motility, and exposing patients to polypharmacy. Microbiota-directed strategies, particularly dietary modification and probiotics, demonstrate promise in reducing arrhythmic risk, whereas early data indicate potential biomarker roles for gut microbial signatures in AF stratification. However, causality remains uncertain, given that most studies are observational with limited sample sizes.

CONCLUSION: The gut-heart axis represents a novel paradigm in AF research. Although preliminary findings support its mechanistic and therapeutic relevance, interventional studies are needed to establish causality and guide clinical application.},
}

@article {pmid41908552,
year = {2026},
author = {Yu, N and Pang, S and Li, Y and Diao, H},
title = {Integrated microbiome-metabolome analysis reveals multiorgan toxicity of 1-nitropyrene and the limited efficacy of ferroptosis inhibitor Fer-1 in rats.},
journal = {Frontiers in toxicology},
volume = {8},
number = {},
pages = {1771766},
pmid = {41908552},
issn = {2673-3080},
abstract = {INTRODUCTION: 1-Nitropyrene (1-NP), a prevalent nitro-polycyclic aromatic hydrocarbon, is increasingly recognized as a potential metabolic disruptor, yet its systemic biological effects remain insufficiently characterized.

METHODS: This study investigated the metabolic, immunological, hepatic, and microbiome alterations induced by chronic 1-NP exposure in rats and assessed whether ferroptosis inhibition via Fer-1 could mitigate these effects.

RESULTS: Although body weight was not significantly altered overall, high-dose exposure impaired growth from week 4. Exposed groups exhibited progressively elevated fasting blood glucose and impaired glucose tolerance, indicating significant disruption of glucose homeostasis. Serum biochemistry revealed dose-dependent reductions in HDL and total cholesterol, while histopathology confirmed hepatocyte ballooning, inflammation, and steatosis consistent with NAFLD-like progression. Hematological changes, including shifts in neutrophil and lymphocyte populations, suggested chronic inflammatory activation. Untargeted metabolomics identified extensive alterations in pathways related to glycolysis, tryptophan metabolism, glycerophospholipid metabolism, and ABC transporters. Gut microbiota analysis demonstrated reduced richness and significant compositional shifts, with functional predictions linking dysbiosis to xenobiotic degradation, lipid metabolism, and phosphotransferase systems. Integrated microbiome-metabolome analysis revealed coordinated disruptions in host-microbial metabolic networks. Fer-1 intervention modified specific metabolic and microbial signatures but did not substantially alleviate major toxic outcomes.

CONCLUSION: Overall, chronic 1-NP exposure causes widespread metabolic injury driven by combined effects on host metabolism, immune regulation, hepatic function, and gut microbial ecology. These findings highlight 1-NP as a potent environmental metabolic disruptor and underscore the need for further mechanistic studies to inform mitigation strategies.},
}

@article {pmid41908560,
year = {2026},
author = {Anand, S and Shete, O and Srivastava, A and Verma, A and Goswami, S and Aggarwal, S and Luthra, K and Ghosh, TS},
title = {Urinary Microbiome Dysbiosis in Children With Congenital Uropathies at Varying Risk for Urinary Tract Infections.},
journal = {Kidney international reports},
volume = {11},
number = {4},
pages = {103799},
pmid = {41908560},
issn = {2468-0249},
abstract = {INTRODUCTION: Febrile urinary tract infections (UTIs) may occur in 30% to 50% of children with vesicoureteral reflux (VUR) or posterior urethral valves (PUVs), frequently leading to renal scarring despite chemoprophylaxis. Approximately 15% of children with uretero-pelvic junction obstruction (UPJO) may develop UTIs. However, investigations that can identify at-risk children before the first episode of UTI are lacking. In this exploratory study, we investigated the preinfection urinary microbiome in Indian children with congenital anomalies of the kidney and urinary tract (CAKUT) to determine whether microbiome alterations, metabolic potential, and antibiotic resistance profiles precede UTI.

METHODS: In this prospective cohort study with follow-up, urine samples were collected from 80 children: 36 with newly diagnosed, antibiotic-naïve CAKUT (18 UPJO, 12 VUR, 6 PUV) and 44 controls. Patients were stratified a priori into low (n = 19) and high-risk (n = 17) groups using clinically defined UTI-susceptibility criteria. V3-V4 16S ribosomal RNA sequencing was used to define urinary microbial profiles. Alpha- and beta-diversity were compared using Shannon index and permutational multivariate analysis of variance (PERMANOVA), respectively. Sliding-window and network-based analyses were used to map dysbiosis gradients. Patients were followed-up longitudinally to assess UTI incidence. Identified dysbiosis-linked microbial markers at baseline were investigated using Kaplan-Meier and Cox-proportional hazard-based analyses as predictors of UTI-risk. Metabolic functions were inferred from taxonomic data. Antibiotic resistance patterns were characterized using the Comprehensive Antibiotic Resistance Database - Resistance Gene Identifier (CARD-RGI) and the World Health Organization Access, Watch, and Reserve classification.

RESULTS: Urinary microbial alpha diversity declined significantly from controls to low-risk to high-risk groups (P = 0.002), accompanied by an increase in intragroup variability (P ≤ 0.005). PERMANOVA revealed distinct clustering by risk (R [2] = 0.11; P = 0.001). Dysbiosis scores inversely correlated with the first Kendall Principal Coordinates Analysis (PCoA) axis (ρ = -0.62; P < 0.001). With increasing risk of UTI, the commensal, control-associated genera declined along this axis while the facultative pathogens became dominant. Control-associated microbiomes favored short- and branched-chain fatty acid and spermidine production; high-risk microbiomes overproduced ammonia, putrescine, and cadaverine. Resistance to 18 of 22 routinely tested antibiotics was almost confined to the 31 risk-associated microbiomes (P = 0.001). During the median (interquartile range) follow-up of 564 (518-594) months, 14 of 36 children with CAKUT developed UTIs, and baseline depletion of health-associated microbial consortia correlated with reduced UTI-free survival. A panel of 10 species-level and 12 genus-level taxa were identified as health-associated markers negatively associated with future UTI-risk during follow-up investigation.

CONCLUSION: Children with CAKUT exhibit urinary microbiome dysbiosis before their first symptomatic UTI, characterized by loss of conserved health-associated taxa, metabolic imbalance, and broad-spectrum antibiotic resistance. These findings support the potential of microbiome-informed, noninvasive risk stratification and microbiome-tailored prophylaxis, while establishing the first Indian pediatric reference set for CAKUT-related UTI prevention.},
}

@article {pmid41908828,
year = {2026},
author = {Zhang, Z and Ku, A and Ji, R and Song, B},
title = {Multi-omics analysis reveals the mechanism of Huaganjian in alleviating cholestatic liver fibrosis.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1744312},
pmid = {41908828},
issn = {1663-9812},
abstract = {Huaganjian (HGJ) is a traditional Chinese medicinal formula with liver-protective effects. However, the pharmacological mechanisms of the effects of HGJ on cholestatic liver fibrosis (CLF) are yet to be clarified. To evaluate the effects of HGJ on CLF and elucidate the underlying mechanisms, C57BL/6J mice were fed a 0.1% 3, 5-diethoxycarbonyl-1, 4-dihydrocollidine (DDC) diet to induce CLF. The efficacy of HGJ was evaluated by measuring the biochemical indicators of liver function, fibrosis, and histology. The underlying mechanisms were investigated using an integrated multi-omics approach, including fecal 16S rRNA sequencing, serum metabolomics, and hepatic transcriptomic analysis. The findings were further validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting (WB). HGJ significantly alleviated liver injury, cholestasis, and fibrosis. Microbiome analysis revealed that Bifidobacterium, Turicibacter, and Clostridium_sensu_stricto_1 abundances were positively correlated with liver injury and fibrosis marker levels, and these abundances decreased following HGJ treatment. Metabolomic analysis identified 531 differential metabolites, including 299 upregulated and 232 downregulated metabolites, following HGJ intervention. Hepatic transcriptomic analysis revealed 164 differentially expressed genes, including 102 upregulated and 62 downregulated genes. Integrated multi-omics analysis revealed that HGJ alleviated CLF by modulating the glycine/serine/threonine metabolism pathway. RT-qPCR and Western blotting experiments confirmed that in this pathway, aminolevulinic acid synthase 1 levels decreased, whereas serine dehydratase and serine dehydratase-like levels increased after HGJ treatment. Overall, HGJ effectively alleviated CLF, and its mechanisms of action were closely linked to the regulation of the glycine/serine/threonine metabolism pathway.},
}

@article {pmid41908923,
year = {2025},
author = {Kurt, Ö and Scanlan, PD and Gentekaki, E and Robertson, LJ and Carmena, D and Dogruman-Al, F and Tsaousis, AD},
title = {The Blastocystis-colorectal cancer hypothesis: correlation is not causation.},
journal = {Open research Europe},
volume = {5},
number = {},
pages = {379},
pmid = {41908923},
issn = {2732-5121},
abstract = {Although superficially persuasive, claims suggesting a causal link between Blastocystis and colorectal cancer (CRC) lack robust scientific support. As Blastocystis is the most common gut protist found in human populations globally, its detection in CRC patients is unsurprising and does not imply pathogenicity. Current claims championing a causal role for Blastocystis in CRC are based on speculative correlations, a single poorly controlled animal study, and inconsistent subtype associations. We argue that linking Blastocystis to CRC is premature, misleading, and may give rise to unnecessary concern in patients that are colonised by or test positive for Blastocystis. We emphasise the need for rigorously designed investigations to establish causal roles for any microorganism in disease and the importance of conclusions being based on solid evidence, particularly in matters of public health.},
}

@article {pmid41909054,
year = {2025},
author = {Hanna, M and Huang, S and Ross, M and Reyes, A and Perera, D and Surathu, A and Cregeen, SJ and Hagan, J and Pammi, M},
title = {Microbiome Signatures and Inflammatory Biomarkers in Culture-Negative Neonatal Sepsis.},
journal = {Applied microbiology (Basel, Switzerland)},
volume = {5},
number = {3},
pages = {},
pmid = {41909054},
issn = {2673-8007},
support = {R03 HD098482/HD/NICHD NIH HHS/United States ; },
abstract = {Overuse of antibiotics is a concern in 'culture-negative sepsis' but it is unclear whether this is due to infection with viruses, fungi or other microbes that are not easily cultured, or whether it results from inflammatory processes. In a prospective study, we enrolled 50 preterm neonates with culture-positive sepsis (CP), culture-negative sepsis (CN), and asymptomatic preterm controls (CO). The microbiome of stool, skin, and blood, including bacterial, viral and fungal components and serum cytokine profiles were evaluated. The microbiome alpha or beta diversity did not differ between CN and CO groups. A MaAsLin analysis revealed increased relative abundances of specific bacterial and fungal genera in stool and skin samples in the CN group compared to CO. The virome analysis identified 24 viruses from skin samples, but they were not statistically different among the three groups. The cytokine and chemokine biomarker profiles were elevated in the CP group but were not statistically different between the CN and CO groups. Although the CN group had a longer hospital stay and higher BPD rates than the controls in unadjusted analyses, these differences were not significant after adjusting for gestational age and birth weight. The CN infants demonstrated microbial shifts without systemic immune activation or significantly worse clinical outcomes, supporting the rationale for discontinuing antibiotics in the absence of positive cultures.},
}

@article {pmid41909172,
year = {2026},
author = {Bao, Y and Xu, K and Du, Y and Feng, M and Li, L and Li, L and Yan, G and Li, X},
title = {PPARγ: a key orchestrator of epidermal barrier, immune responses, and lipid metabolism in atopic dermatitis pathogenesis and therapy.},
journal = {Frontiers in allergy},
volume = {7},
number = {},
pages = {1780908},
pmid = {41909172},
issn = {2673-6101},
abstract = {Atopic dermatitis (AD) is an immune-mediated inflammatory dermatosis characterized by epidermal barrier dysfunction, immune dysregulation, and cutaneous microbial dysbiosis. Existing therapeutic modalities for AD are limited in efficacy and durability, highlighting an unmet clinical need for novel, safe, and effective treatment strategies. Peroxisome proliferator-activated receptor gamma (PPARγ), a pivotal nuclear receptor involved in metabolic and inflammatory regulation, has emerged as a promising therapeutic target for AD. Its pleiotropic mechanisms encompass the restoration of stratum corneum integrity, modulation of aberrant immunoinflammatory signaling, normalization of cutaneous lipid metabolism, and regulation of the cutaneous microbiome and neuroimmune circuitry. This review comprehensively synthesizes the mechanistic evidence linking PPARγ to AD pathogenesis and critically appraises its potential as a novel therapeutic.},
}

@article {pmid41909251,
year = {2026},
author = {Sun, F and Yuan, M and Liao, C and Sun, Y and Yu, L and Zhuo, Y and Peng, Y and Tang, X and Zeng, Q and Song, J and Tao, X and Li, Q and Chen, M and Zhang, Y},
title = {Optimizing flue-cured tobacco planting patterns: enhanced rhizosphere nutrient availability and microbial community dynamics.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1735540},
pmid = {41909251},
issn = {1664-302X},
abstract = {INTRODUCTION: Continuous monoculture of flue-cured tobacco causes soil degradation and microbial dysbiosis. While crop rotation can alleviate these obstacles, how different cropping patterns regulate soil carbon (C) and nitrogen (N) metabolic functions remains unclear.

METHODS: A four-year field experiment compared tobacco monoculture (CK), tobacco-maize rotation (TM), tobacco-rice rotation (TR), and tobacco-sweet potato intercropping (TP). Soil physicochemical properties, enzyme activities, metagenomic sequencing, and microbial network analysis were integrated.

RESULTS: TR significantly improved soil health: pH (+6.6%), organic matter (+22.1%), and urease activity (+12.5%). It enriched beneficial microbes (Pseudomonadota +16.4%, Mucoromycota +327%) and upregulated C-cycle (korA +42.3%) and N-assimilation genes (amoC +460%), while suppressing denitrification (nirK). TM increased available P/K but enriched oligotrophic taxa and reduced sucrase activity. TP triggered pathogenic fungi (Olpidium +160%), depleted beneficial microbes, and broadly suppressed C/N metabolic genes (cbbL -94.5%, nirS -21.8%).

DISCUSSION: Cropping patterns differentially reshape microbial communities and metabolic functions, determining their efficacy against continuous cropping obstacles. TR establishes efficient C/N cycling with "high assimilation, low denitrification," whereas TP induces pathogenic proliferation and metabolic suppression. This provides a functional framework for designing cropping systems to enhance soil health and tobacco productivity.},
}

@article {pmid41909261,
year = {2026},
author = {Choi, J and Shim, K and Bae, GS and Jeon, E and Hwang, EH and Kim, G and Baek, SH and Hong, JJ and Kim, DS and Kim, SH and Koo, BS},
title = {Comparative analysis of gut microbiota and host phenotypic characteristics across enterotype-like clusters in cynomolgus and rhesus macaques.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1775757},
pmid = {41909261},
issn = {1664-302X},
abstract = {Microbiome has been increasingly recognized for its close association with host physiology and diseases. Due to their close genetic relatedness to humans and standardized environmental conditions, captive macaque species serve as the most evolutionarily comparable preclinical animal models for studying human microbiome research. However, the characterization of gut microbiota and host phenotypic traits within each enterotype-like cluster of macaque species remains poorly understood. We analyzed microbiome characteristics and host metadata within enterotype-like clusters of cynomolgus and rhesus macaques housed in the same facility but with different origins of birth. At the phylum level, Bacteroidota, Firmicutes, Spirochaetota, and Proteobacteria were predominantly observed in both species. Except for Fibrobacterota at the phylum level, no significant interspecies differences were observed in bacterial composition or alpha diversity across taxonomic levels. Based on a prevalence threshold of 90%, cynomolgus macaques were found to share 12.4% of genera, while rhesus macaques shared 18.2%. Based on the relative abundance patterns of the genera Prevotella 9, Rikenellaceae RC9 gut group, and Treponema, the fecal microbiome of cynomolgus macaques was classified into three enterotype-like clusters (cluster 1, cluster 2, and cluster 3) whereas that of rhesus macaques was classified into two enterotype-like clusters. Using linear mixed-effects models, we identified species-specific associations between enterotype-like clusters and host phenotypes. In cynomolgus macaques, clustering was primarily associated with hematological and selected biochemical parameters, whereas in rhesus macaques, enterotype-like clusters were limited to body weight and hemoglobin. Despite a standardized diet and shared environments, distinct clusters and pronounced microbial individuality associated with birthplace suggest that early-life colonization is a key determinant of long-term gut microbiome structure and host phenotypes in captive primates. Also, identifying enterotype-like clusters in NHPs prior to analysis is essential for accurate and relevant human microbiome modeling, since each cluster may correspond to distinct human enterotypes and phenotypic traits.},
}

@article {pmid41909266,
year = {2026},
author = {Zhu, Z and Li, X and Cui, T and Chen, Z and Liu, Y and Chen, X and Tian, Y and Mu, Y and Wu, Y and Ji, Q and Yan, S and Cheng, Y},
title = {Temporal heterogeneity of microbial ecosystems and its formation mechanisms in Moutai-flavor Baijiu fermentation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1798174},
pmid = {41909266},
issn = {1664-302X},
abstract = {The influence of workshop age on Moutai-flavor Baijiu fermentation is recognized, but the mechanisms driving microbial community shifts remain unclear. Understanding how the physical environment selects for specific microbiota is crucial for optimizing new workshops. Through 16S/ITS sequencing of pit-entry fermented grains, Daqu, air, and cooling yards in 5-, 10-, 20-, and 30-year-old workshops, Lactobacillus emerged as a key discriminant genus, increasing from 15.02% (5-year) to 35.59% (30-year). SourceTracker analysis revealed the cooling yard as the primary microbial source, contributing 54.2% on average to fermented grains. CO2-TPD analysis showed a 3.6-fold reduction in cooling yard surface basicity (from 0.11 to 0.03 mmol·g[-1]) over 30 years, resulting in high abundances (>10%) of alkalotolerant bacteria (e.g., Alkalibacterium, Nesterenkonia) and low Lactobacillus (2.17%). Nesterenkonia was also a biomarker in 5-year fermented grains. This confirms cooling yard surface basicity drives microecological differences, revealing how long-term production practices domesticate microbial communities and providing a theoretical basis for new workshop adaptation.},
}

@article {pmid41909643,
year = {2026},
author = {Yao, Y and Hu, X and Li, R and Tan, Z and Yu, H and Lin, Z and Zhang, T and Habimana, O},
title = {Probiotic yeast engineers a protective biofilm environment to enhance bioremediation and seahorse health in aquaculture.},
journal = {Biofilm},
volume = {11},
number = {},
pages = {100357},
pmid = {41909643},
issn = {2590-2075},
abstract = {Sustainable animal farming via intensive aquaculture relies on a balanced microbial ecosystem that promotes animal well-being. This research explored the use of the probiotic yeast Saccharomyces boulardii to influence tank biofilm microbiomes for improving the health of lined seahorses, Hippocampus erectus. Following a severe mortality event at week 6 that affected both groups, the control group demonstrated partial recovery to 71.4% survival, whereas the probiotic group achieved a higher survival, with a final rate of 88.9% after a disease challenge. This recovery led to a notable reduction in enteritis occurrences with a significant increase in average body weight and a 3.9-fold increase in activity compared to control conditions. Shotgun metagenomic analysis indicated that the enhancements were significantly supported by a marked reorganization of the tank's biofilm community. Probiotic supplementation significantly reduced microbial diversity and selected for a beneficial consortium enriched in taxa with recognized roles in nutrient cycling, including Rhodobacterales (involved in sulfur cycling and pathogen antagonism) and Pirellulaceae (key in polysaccharide breakdown). This engineered biofilm has greater genetic potential for energy generation, glucose degradation, and inorganic ion transfer. Crucially, virulence factor genes and pathogen-associated sequences were substantially suppressed in probiotic-treated biofilms. Our research shows that S. boulardii acts as a crucial modulator, creating a protective biofilm that boosts bioremediation while decreasing pathogenic threats. This ecological approach to the application of probiotics (targeting the environmental rather than host-associated microbiome) may offer a sustainable means to promote health and resilience within aquaculture systems.},
}

@article {pmid41909648,
year = {2026},
author = {Kumar, V and Das, BK and Roy, S and Bhowal, P and Roy, A and Bruce, TJ and Galindo-Villegas, J},
title = {Exploring the host-pathogen interaction and genome analysis of multidrug-resistant bacterial pathogen Proteus penneri isolated from Labeo rohita.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1733414},
pmid = {41909648},
issn = {1664-3224},
mesh = {Animals ; *Fish Diseases/microbiology/immunology ; *Drug Resistance, Multiple, Bacterial/genetics ; *Host-Pathogen Interactions/genetics ; *Cyprinidae/microbiology/immunology ; Phylogeny ; *Proteus Infections/microbiology/veterinary/immunology ; *Genome, Bacterial ; Anti-Bacterial Agents/pharmacology ; Virulence ; Genomics ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Multidrug-resistant (MDR) bacterial pathogens represent an escalating challenge to sustainable aquaculture, particularly in high-value freshwater species such as Labeo rohita, a cornerstone of South Asian aquaculture. This study provides the first comprehensive integration of genomic, immunological, and microbiome analyses to characterize Proteus penneri as an emerging MDR pathogen associated with severe disease manifestations in L. rohita, including exophthalmia, ulceration, and hemorrhage. Robust identification through biochemical assays, 16S rRNA sequencing, and phylogenetic analysis confirms the clinical relevance of this isolate. Functional assays demonstrated pronounced virulence, evidenced by hemolysin activity, extensive histopathological damage, and dose-dependent mortality, underscoring its pathogenic capacity in vivo. The observed resistance to multiple frontline antibiotic classes, including tetracyclines, macrolides, and carbapenems, highlights a critical therapeutic limitation in aquaculture settings. Genomic analysis further revealed a diverse repertoire of antimicrobial resistance genes, virulence determinants (notably biofilm formation and secretion systems), and mobile genetic elements, suggesting a strong potential for persistence, adaptability, and horizontal gene transfer. Infection-associated gut microbiome disruption, marked by elevated MAR indices and enrichment of virulence-associated taxa, indicates that P. penneri not only exploits host tissues but also reshapes the microbial ecosystem in ways that may exacerbate disease severity and resistance dissemination. Concurrently, heightened serum cortisol, C3, and Hsp70 levels, along with transcriptional upregulation of key immune and stress-related genes (hsp70, nod, il6, sod, c3, and myd88), reflect an intense pro-inflammatory and physiological stress response. In silico docking analyses implicating myd88-lipopolysaccharide interactions provide mechanistic insight into potential immune-modulatory strategies employed by the pathogen. Collectively, these findings delineate a multifactorial basis for P. penneri virulence and MDR, emphasizing its significance as an emerging aquaculture pathogen. Future research should prioritize functional validation of key virulence and resistance genes, longitudinal surveillance to assess transmission dynamics and AMR spread, and experimental evaluation of alternative disease mitigation strategies, including probiotics, phage therapy, and immune-modulating interventions, to reduce antibiotic reliance and enhance fish health resilience in aquaculture systems.},
}

Animals
*Fish Diseases/microbiology/immunology
*Drug Resistance, Multiple, Bacterial/genetics
*Host-Pathogen Interactions/genetics
*Cyprinidae/microbiology/immunology
Phylogeny
*Proteus Infections/microbiology/veterinary/immunology
*Genome, Bacterial
Anti-Bacterial Agents/pharmacology
Virulence
Genomics
RNA, Ribosomal, 16S/genetics

@article {pmid41909844,
year = {2026},
author = {Lin, B and Tong, S and Ba, C and Wang, X},
title = {Precision treatment of gastrointestinal tumours and liver disease interaction mechanisms based on multi-omics data and microbiome hubs.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1791531},
pmid = {41909844},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Neoplasms/therapy/microbiology ; *Gastrointestinal Microbiome ; *Liver Diseases/therapy/microbiology ; *Precision Medicine/methods ; Genomics/methods ; Proteomics/methods ; Metabolomics/methods ; Tumor Microenvironment ; Carcinogenesis ; Multiomics ; },
abstract = {The global prevalence of gastrointestinal tumours and the bottlenecks in their diagnosis and treatment are being systematically overcome by the multi-omics revolution: high-throughput technologies are driving the multidimensional integration of genomics-transcriptomics-proteomics-metabolomics to comprehensively decode the genetic architecture of tumours. Meanwhile, the gut microbiota, acting as a core regulatory hub, drives carcinogenesis through immune microenvironment remodelling and metabolic pathway hijacking, further facilitating proteome-metabolome multidimensional integration, comprehensively decoding tumour genetic architecture. The gut microbiota, acting as a core regulatory hub, drives carcinogenesis through immune microenvironment remodelling and metabolic pathway hijacking, while mediating a vicious cycle network linking liver disease and tumours via the gut-liver axis. This review examines the application of multi-omics technologies in gastrointestinal tumour research, summarises the role of gut microbiota in tumourigenesis and its interaction with liver disease, and envisions future interventions targeting the gut microbiome for early disease diagnosis and precision treatment.},
}

Humans
*Gastrointestinal Neoplasms/therapy/microbiology
*Gastrointestinal Microbiome
*Liver Diseases/therapy/microbiology
*Precision Medicine/methods
Genomics/methods
Proteomics/methods
Metabolomics/methods
Tumor Microenvironment
Carcinogenesis
Multiomics

@article {pmid41909873,
year = {2026},
author = {Yu, J and Baek, H and Jaiswal, V and Park, M and Lee, HJ},
title = {Heavy metal accumulation and fecal microbiota response in black soldier fly larvae: identification of Leminorella grimontii as a potential indicator species.},
journal = {Food science and biotechnology},
volume = {35},
number = {5},
pages = {1329-1338},
pmid = {41909873},
issn = {2092-6456},
abstract = {UNLABELLED: With growing environmental concerns about marine pollution from heavy metals, black soldier fly larvae (BSFL) are gaining attention for their potential use in sustainable waste-to-feed systems. In this study, BSFL were raised on diets containing cadmium (Cd), lead (Pb), mercury (Hg), and arsenic (As) to assess their growth, metal accumulation patterns, and changes in microbiota. While Cd mainly accumulated in the larval body, Pb, Hg, and As were primarily excreted through exuviae and feces. This pattern remained consistent even when larvae were fed naturally contaminated mackerel heads. Microbiome analysis of fecal samples showed that Leminorella grimontii had a strong positive correlation with Hg and As concentrations, suggesting its potential as a microbial indicator species for heavy metal exposure. These findings support the use of BSFL in bioconversion systems and suggest L. grimontii as a new biomarker for environmental monitoring.

GRAPHICAL ABSTRACT: Scheme 1Experimental procedure and fecal microbiome results.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10068-026-02114-y.},
}

@article {pmid41909880,
year = {2025},
author = {Cold, F and Heintz, JE and Ghathian, KSA and Stenbøg, PA and Hansen, LH and Carstens, AB and Petersen, AM and Halkjaer, SI and Bendtsen, F and Ytting, H},
title = {Low incidence of cytolysin-positive E. faecalis and no correlation to survival in Danish patients with alcohol-associated hepatitis: A prospective cohort study.},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2549729},
pmid = {41909880},
issn = {2993-3935},
abstract = {Alcohol-associated hepatitis (AH) is a severe and life-threatening form of alcohol-associated liver disease with no approved treatments for reducing long-term mortality. Cytolysin-producing E. faecalis in the gut microbiota of AH patients has been reported as highly correlated to mortality. We investigated whether we could reproduce this correlation in a cohort of Danish patients with AH. Fecal samples from 28 hospitalized patients with AH were analyzed for cytolysin-producing E. faecalis and were followed for 1 y after hospital admission. The primary endpoint was comparison of 180-d mortality in AH patients with and without cytolysin-positive fecal samples. Three of twenty-eight (10.7%) fecal samples were identified as cytolysin-positive. There were no significant differences at baseline between cytolysin-positive and -negative patients in terms of age, Glasgow Alcoholic Hepatitis Score, Charlson Comorbidity Index or biochemical variables (INR, bilirubin, albumin). There was no difference in mortality between the groups 180 d after hospital admission; one of the three (33%) cytolysin-positive patients had died compared to 9 of the 25 (36%) cytolysin-negative (p-value for difference = 1.0). We report a low incidence of cytolysin-positive E. faecalis in hospitalized Danish AH patients and no greater risk of mortality compared to cytolysin-negative AH patients.},
}

@article {pmid41909881,
year = {2025},
author = {Liu, W and An, M and Wang, Q and Liu, Y and Shang, Y and Dong, X and Ding, H and Fu, S and Han, X and Shang, H},
title = {Gut microbiome-induced metabolites promote the role of Silybin as adjunctive drug in HIV-positive immunological nonresponders.},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2569789},
pmid = {41909881},
issn = {2993-3935},
abstract = {HIV-infected immunological nonresponders (INRs) endure persistent T-cell dysfunction and chronic inflammation, facing high risk of various complications and mortality, with no effective therapies available. Silybin, the principal constituent of a plant extract, possesses anti-inflammation and immunomodulatory properties. The gut microbiome has been shown to modulate the efficacy of immune therapies and drugs. We gave 54 INRs oral silybin for three months and used multi-omics to investigate the gut-related factors influencing the efficacy of silybin. Silybin raised CD4[+] T cells counts in 52% of participants and an efficacy classification model based on baseline gut microbiome and metabolites was developed. Favorable gut bacteria produced anti-inflammatory metabolites that downregulated Ras/MAPK/PI3K-Akt signaling pathways also targeted by silybin. Our findings shed light on a novel therapeutic approach for addressing immune dysfunction in HIV-positive INRs and have important implications for personalized medical strategies in the management of HIV infection.},
}

@article {pmid41909883,
year = {2025},
author = {Abubakar, D and Abdullahi, H and Ibrahim, I},
title = {Bridging Microbiomes: Exploring Oral and Gut Microbiomes in Autoimmune Thyroid Diseases- New Insights and Therapeutic Frontiers.},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2452471},
pmid = {41909883},
issn = {2993-3935},
abstract = {Autoimmune thyroid diseases (AITDs) are the most common organ-specific autoimmune disorders characterized by thyroid dysfunction and immune system deficiencies. In recent decades, the role of the microbiome in autoimmune diseases has gained increasing attention, with emerging research linking gut microbiome alterations to the development of AITDs. This review summarizes current knowledge on the relationship between AITDs and the gut microbiome. Additionally, it emphasizes the role of the oral microbiome in AITDs, an area often overlooked in autoimmune research. Beyond the microbiome, the virome and mycobiome have been recognized as critical but underexplored components of the human microbiome, potentially contributing to immune dysregulation and the pathogenesis of AITDs. The review also explores modulating the microbiome for managing AITDs, including diet adjustment, the potential use of probiotics, postbiotics, symbiotics, and even fecal microbiota transplantation (FMT) to restore a balanced microbiome that may positively influence the immune system and, by extension, the course of AITDs. This review thoroughly explores the intricate relationship between AITDs, the gut, and oral microbiomes, paving the way for precision medicine applications in AITDs. Examining microbiota-thyroid interactions highlights the potential for targeted, personalized treatments and novel therapeutic therapies, guiding future therapeutic strategies for more effective and precisely tailored AITD management approaches.},
}

@article {pmid41909884,
year = {2025},
author = {Pateriya, D and Prasoodanan P K, V and Scaria, J and Sharma, VK},
title = {Landscape of flavonoid metabolism in human gut microbiome and its association with health and disease.},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2520788},
pmid = {41909884},
issn = {2993-3935},
abstract = {The positive effects of dietary flavonoids on health depend on their bioavailability in the human gut, where the flavonoid-modifying enzymes (FMEs) in gut bacteria play a crucial role in flavonoid metabolism. Thus, to comprehensively examine the role of FMEs in this process, we first constructed a database of potential FMEs containing 6,865 proteins. We identified homologs of these FMEs in gut bacterial genomes and reported species that can potentially modify flavonoids but were not previously known in this context. We examined the differential abundance of FMEs in the gut microbiomes of healthy and diseased individuals from Western and non-Western populations with distinct dietary habits. The differential enrichment of key FMEs between Western and non-Western populations and between disease and healthy samples highlights differences in gut flavonoid metabolism based on diet, population, and health status. This study reveals a comprehensive landscape of flavonoid metabolism in the human gut microbiome.},
}

@article {pmid41909885,
year = {2025},
author = {Lau, RI and Wong, MCS and Lau, LHS and Lau, AYL and Mak, IWC and Lo, OSH and Chan, NN and Dai, DLK and Hau, KC},
title = {Role of gut microbiome in pathogenesis and treatment of diseases: Multidisciplinary experts' opinion of the Asian Medical Experts Academy (AMEA).},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2558575},
pmid = {41909885},
issn = {2993-3935},
abstract = {Emerging evidence suggests the role of the gut microbiome in the health and diseases of multiple organs and systems. In the past decade, an increasing trend in the use of microbiome-based therapeutics (e.g., probiotics, prebiotics, synbiotics) has been observed in Asia and globally. However, local and global clinical guidelines on the use of microbiome-based therapeutics are limited. A multidisciplinary working group has been established to foster communication between experts from diverse medical specialties on the clinical application of microbiome-based therapeutics. Through conducting an extensive review on current evidence on the importance of the gut microbiome and the potential use of microbiome-based therapeutics in health and diseases, the experts' working group identified the unmet needs related to the use of microbiome-based therapeutics in the clinical settings in Asia and global contexts. Thirteen position statements were developed, including eight statements focusing on the role of the gut microbiome in health and disease pathogenesis, as well as six statements focusing on the potential clinical applications. A list of potential indications for microbiome-based therapeutics was also proposed based on current evidence and clinical experience. This paper is intended to serve as a reference that assists healthcare professionals in improving care for patients using microbiome-based therapeutics in Asia and globally.},
}

@article {pmid41909889,
year = {2025},
author = {Lan, Z and Chen, J and Lan, S and Li, N and Yang, B and Hou, J and Yang, X},
title = {Hydrogen-rich water attenuates radiation-induced oral mucositis in mice via antioxidant and gut microbiota-stabilizing effects: a longitudinal study.},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2595392},
pmid = {41909889},
issn = {2993-3935},
abstract = {Radiation-induced oral mucositis (RIOM) frequently complicates head and neck radiotherapy, leading to severe pain, compromised nutrition, and often requiring treatment modifications. Although craniofacial-only irradiation is confined to the head and neck region, it can still disrupt gut homeostasis. Mice subjected to head and neck irradiation developed marked epithelial damage in both the oral and intestinal mucosa, as evidenced by pronounced RIOM and diminished barrier integrity. Histological examination revealed substantial mucosal thinning and leukocyte infiltration in the tongue, along with reduced occludin and ZO-1 expression in colonic tissues. Supplementation with hydrogen-rich water (HW) markedly decreased the severity of oral lesions and preserved epithelial thickness, while restoring the expression of tight junction proteins in the colon. Fecal 16S rRNA sequencing showed that radiation alone provoked expansions of Streptococcus and Helicobacter, coupled with a decline in short-chain fatty acid-producing families (Lachnospiraceae, Ruminococcaceae). In contrast, HW supplementation partially reversed these microbial shifts, which correlated with reduced oral inflammatory markers. Collectively, these findings underscore an oral-gut axis whereby HW fosters mucosal healing through microbiome stabilization and decreased inflammatory stress, suggesting that HW as a promising adjunct for managing head and neck irradiation-related complications.},
}

@article {pmid41909890,
year = {2025},
author = {Park, G and Oh, S and Kim, M and Jeong, Y and Kim, G},
title = {Common microbial signatures in blood and their amplification in clinical disorders.},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2473450},
pmid = {41909890},
issn = {2993-3935},
abstract = {Blood microbiome research has emerged as a significant area of study, exploring microbial signatures within the bloodstream and their potential implications for various clinical disorders. This study aimed to identify common microbial signatures in blood across cohorts and investigate how these signatures are altered in clinical conditions. We conducted a meta-analysis of 15 publicly available studies utilizing amplicon sequencing, including 687 control and 651 case individuals with various disorders from diverse geographic locations to compare their blood microbiome profiles. The results revealed that most microbes detected in the blood originated from the gut, oral cavity, and skin, with several genera such as Corynebacterium, Streptococcus, and Lactobacillus consistently identified across studies. Furthermore, we observed a significant increase in microbial diversity and abundance in individuals with clinical disorders compared to the control group. Notably, microbial genera originating from the gut and oral cavity, including Acinetobacter, Prevotella, and Clostridium sensu stricto-1, were more prevalent in disease cohorts, suggesting a potential link between the translocation of microbial signatures and disease pathology. The study underscores the importance of considering microbial signatures as potential biomarkers in clinical settings and calls for further investigation into the role of circulating microbial DNA in immune response and disease progression.},
}

@article {pmid41909891,
year = {2025},
author = {Manzoor, H and Kayani, MUR},
title = {Insights into the gut microbiome-metabolite dynamics in breast cancer.},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2483446},
pmid = {41909891},
issn = {2993-3935},
abstract = {In recent years, understanding the intricate connection between gut microbiome and cancer development has gained significant attention. The gut microbiome has a key role in maintaining overall human health and modulating the body's defense mechanism against various diseases. This review examines the multifaceted association between the gut microbiome and breast cancer, providing a comprehensive overview of studies from the last two decades that investigate both anti-cancer and pro-cancer properties of gut metabolites. Compounds such as nisin, inosine, acetate, propionate, and conjugated linoleic acids have demonstrated potential as therapeutic agents against breast cancer, while others, including butyrate, lactate, certain bile acids, and secondary metabolites, exhibit dual roles, showing both anti-cancer and pro-cancer properties under different conditions, with some implicated in tumor progression. Moreover, emerging research highlights the dual roles of these metabolites in influencing the efficacy of conventional breast cancer therapies. Despite promising evidence, the molecular mechanisms underlying these opposing actions remain unclear and require further investigation. To advance our understanding, future research should prioritize elucidating these mechanisms, establishing dose-response relationships, and conducting animal and clinical studies to validate in vitro findings. This review also identifies key gaps and highlights potential directions for future research in this field.},
}

@article {pmid41909893,
year = {2025},
author = {Jorgensen, JA and Choo-Kang, C and Wang, L and Issa, L and Gilbert, JA and Ecklu-Mensah, G and Luke, A and Bedu-Addo, K and Forrester, T and Bovet, P and Lambert, EV and Rae, D and Argos, M and Kelly, TN and Sargis, RM and Dugas, LR and Dai, Y and Layden, BT},
title = {Toxic metals impact gut microbiota and metabolic risk in five African-origin populations.},
journal = {Gut microbes reports},
volume = {2},
number = {1},
pages = {2481442},
pmid = {41909893},
issn = {2993-3935},
abstract = {Underlying mechanisms by which exposures to toxic metals/metalloids impact obesity and type 2 diabetes (T2DM) risk remain largely unknown. Gut microbiota have been strongly associated with cardiometabolic risk. To assess relationships between high metal exposures, gut dysbiosis, and metabolic dysregulation, we analyzed associations among gut microbiome taxa, dichotomized metal levels (arsenic, lead, mercury, cadmium), clinical measures (BMI, fasting blood glucose, blood pressure), and diagnoses (hypertension, obesity, diabetes) in 178 African-origin adults (52% female, mean age = 43.0 ± 6.4 years) from Ghana, South Africa, Jamaica, Seychelles, and USA. High vs. low lead and arsenic levels had a significant effect on beta diversity (p < 0.05). Seventy-one taxa were associated with high lead levels: 30 with elevated BMI, 22 with T2DM, and 23 with elevated fasting blood glucose (p < 0.05); 115 taxa were associated with high arsenic levels: 32 with elevated BMI, 33 with T2DM, and 26 with elevated blood glucose (p < 0.05). Porphyrin metabolism was the most enriched metabolic pathway in taxa associated with higher lead and arsenic exposure. These data provide the first findings from African-origin adults that demonstrate the association between the gut microbiome with lead and arsenic exposure and obesity and T2DM risk.},
}

@article {pmid41900768,
year = {2026},
author = {Zhou, S and Xu, Z and Shen, J},
title = {Female Reproductive Tract Organ-on-Chips: Modeling Barrier Function and Drug Transport.},
journal = {Pharmaceutics},
volume = {18},
number = {3},
pages = {},
pmid = {41900768},
issn = {1999-4923},
support = {1U01FD007656//United States Food and Drug Administration/ ; 33040//Massachusetts Life Sciences Center/ ; },
abstract = {Female reproductive tract (FRT) disorders such as maternal conditions and gynecological cancers represent a significant global health burden. However, women's health, and particularly locally acting therapies targeting the FRT, has historically been underprioritized in drug development and translational research. Developing safe and effective therapies requires a clear understanding of drug transport across FRT barriers. Conventional in vitro culture systems and animal studies fail to recapitulate the physiological complexity of the human FRT, including stratified mucosal architecture, functional mucus barriers, microbiome interactions, as well as dynamic hormonal regulation. Recently, organ-on-chip (OoC) microfluidic platforms, integrating human cells with precisely controlled perfusion, have emerged as advanced in vitro systems capable of recreating dynamic physiological microenvironments. This review summarizes the major anatomical and physiological barriers of the FRT, including the vagina, cervix, endometrium, and placenta, and discusses critical design considerations for the development of FRT-on-chip models. We highlight the advanced OoC developed to study infection, drug permeation, hormonal responses, and maternal-fetal interface dynamics. Finally, future perspectives are outlined, including the integration of immune components, vascularization strategies, and multi-organ systems to better simulate inter-organ communication. Collectively, these advances underscore the potential of FRT-on-chip models as predictive platforms for preclinical drug screening, toxicity evaluation, and personalized medicine.},
}

@article {pmid41900770,
year = {2026},
author = {Vadlapatla, R and Shirazi, AN and Koomer, A and Weng, J and Ghilarducci, ME and Qudus, A and Parang, K},
title = {Microbiome-Responsive Hydrogels: From Biological Cues to Smart Biomaterials.},
journal = {Pharmaceutics},
volume = {18},
number = {3},
pages = {},
pmid = {41900770},
issn = {1999-4923},
abstract = {Background: Stimuli-responsive hydrogels (SRHs) are smart polymeric materials that undergo reversible physicochemical changes in response to abiotic cues and externally applied fields, enabling applications in drug delivery, wound healing, and tissue engineering. However, they exhibit limited biological specificity and do not adequately reflect the dynamic, disease-relevant complexity of native tissue microenvironments. Microbe-colonized tissues display distinctive biochemical features driven, shaped by microbial metabolism, including localized pH gradients, short-chain fatty acid production, secretion of quorum-sensing molecules, biofilm formation, and expression of specialized enzymes. These endogenous, spatiotemporally regulated signals are closely linked to host physiology and pathology but remain underutilized in hydrogel design. This review aims to highlight microbiome-responsive hydrogels (MRHs) as a strategy to address this gap. Methods: This study summarizes current engineering approaches, key microbial stimuli, and emerging biomedical applications of MRHs, with emphasis on translational and regulatory challenges. Results: Microbiome-responsive hydrogels (MRHs) address this gap by leveraging microbial metabolic and biochemical cues to induce swelling, degradation, drug release, antibacterial activity, or structural transformation. By directly coupling to microbe-derived stimuli, MRHs offer improved physiological relevance, enhanced local specificity, and new opportunities for precision therapy targeting disease-associated microbial niches. Conclusions: Despite their promise, MRHs remain an early and fragmented field, lacking standardized biological triggers, material design frameworks, and performance evaluation strategies. This review summarizes current engineering approaches, key microbial stimuli, and emerging biomedical applications, with emphasis on translational and regulatory challenges, positioning MRHs as an underexplored platform for next-generation smart biomaterials.},
}

@article {pmid41900857,
year = {2026},
author = {Shah, IM and Lebrilla, CB and German, JB and Mills, DA},
title = {Selective Human-Milk-Inspired Antimicrobial Peptides for the Treatment of Bacterial Vaginosis.},
journal = {Pharmaceutics},
volume = {18},
number = {3},
pages = {},
pmid = {41900857},
issn = {1999-4923},
support = {R43AI165105/GF/NIH HHS/United States ; },
abstract = {Background: Antimicrobial resistance (AMR) is a global healthcare threat. Traditional largely non-selective antibiotics produce side effects due to the natural host microbiome being modified creating a loss in homeostasis. In women, AMR is a cause of acute generational impact. For example, bacterial vaginosis (BV), the most common gynecological infection in reproductive-age women, is a serious public health concern due to its high rates of recurrence, secondary infections, and reproductive issues; and two currently prescribed antibiotics for BV do not fully resolve the symptoms. Objective: The strong need for innovative, potent, safe, and selective therapeutics has prompted a search for such bioactive molecules in milk. Resulting from 200 million years of evolutionary pressure, mammalian lactation not only nourishes infants, but it has also been under relentless Darwinian selective pressure to provide protection from a variety of infections. Methods: Computationally designed human-milk-inspired peptides (AMPs) were tested in standard microbicidal assays for activity against BV pathogens, and evaluated for stability and safety. Results: Several AMPs are bactericidal towards Gardnerella vaginalis, a major BV-associated pathogen, and other BV-associated pathogens. Some novel AMPs do not impact the viability of key lactobacilli linked to a healthy vaginal microbiome. These stable, membrane-acting cationic AMPs reduce inflammation during an infection assay and are safe in EpiVag organoid tissues. Conclusions: AMPs can address concerns like non-selectivity and antibiotic resistance-thereby addressing AMR. Lead AMPs from this study offer a promising solution for the development of novel therapeutics for the treatment of BV, which may reduce the burden of AMR.},
}

@article {pmid41900935,
year = {2026},
author = {Santaniello, U and Mastorino, L and Pala, V and Rosset, F and Crespi, O and Quaglino, P and Ribero, S},
title = {Pharmacomicrobiomics in Psoriasis: Microbiome-Drug Interactions Across Systemic Treatments.},
journal = {Life (Basel, Switzerland)},
volume = {16},
number = {3},
pages = {},
pmid = {41900935},
issn = {2075-1729},
abstract = {Psoriasis is a chronic immune-mediated skin disease with highly variable responses to systemic therapies. Emerging evidence highlights the microbiome as a potential modulator of drug efficacy and toxicity. Gut bacteria can enzymatically metabolize drugs, such as methotrexate, altering bioavailability and therapeutic outcomes, while microbial metabolites-including short-chain fatty acids, branched-chain amino acids, and tryptophan derivatives-shape host immunity and barrier integrity, influencing drug action. Baseline microbial signatures have been linked to treatment response, potentially predicting anti-TNF or IL-17 inhibitor efficacy. Systemic therapies themselves reshape microbial communities: IL-17 blockade induces broad shifts in gut and skin microbiota, whereas cyclosporine and anti-TNF agents exert subtler effects. Small molecules such as apremilast and fumarates may reduce fungal overgrowth and influence microbial composition, whereas data on JAK/TYK2 inhibitors remain limited. Notably, current evidence exhibits a literature bias toward the gut microbiota, while the roles of the oral and skin axes remain understudied. Adjunctive microbiome-directed interventions, including probiotics and fecal microbiota transplantation, have demonstrated potential to enhance treatment outcomes by promoting anti-inflammatory taxa and restoring barrier function. Despite these promising findings, current evidence is heterogeneous, often limited by small sample sizes, short follow-up, and variable methodology. Integrating pharmacomicrobiomics data with clinical, genetic, and multi-omics profiling could enable precision medicine approaches in psoriasis, allowing therapy selection tailored to individual microbial and metabolic signatures. Future research should focus on longitudinal, multicenter studies to identify actionable microbial biomarkers, clarify mechanistic interactions between drugs, microbes, and host immunity, and evaluate microbiome-targeted adjuncts in randomized trials. Understanding the bidirectional crosstalk between systemic therapies and the microbiome may transform psoriasis management, improving efficacy, reducing adverse events, and enabling durable, personalized responses.},
}

@article {pmid41901063,
year = {2026},
author = {Nunna Sai Venkata, L and Mishra, AK and Mohanta, YK and Rustagi, S and Bahuguna, A and Tomar, A and Baek, KH and Mishra, B},
title = {The Gut Gambit: A Review of How Microbial Imbalance Fuels Metabolic Mayhem.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901063},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/microbiology/metabolism ; Oxidative Stress ; *Metabolic Diseases/microbiology/metabolism ; Epigenesis, Genetic ; Probiotics ; Inflammation/microbiology ; Animals ; },
abstract = {BACKGROUND/OBJECTIVES: An imbalance in gut microbiota, known as gut dysbiosis, results in reactive oxygen species overproduction, which can cause inflammatory conditions, damage DNA, trigger immunity, and induce epigenetic modifications of crucial genes that regulate metabolic pathways. Such a condition can also weaken the resilience of the protective gut wall and elevate colon permeability, allowing toxins from the gut to reach the liver and bloodstream, contributing to oxidative damage, autoimmune diseases, and epigenetic changes linked to metabolic disorders.

METHODS: The Scopus database was exclusively searched for the literature. Relevant articles were identified using predefined keywords, including gut dysbiosis, microbiota, microbiome, oxidative stress, metabolic disorders, inflammation, and epigenetics or combinations. Gut microbiota- and diet-induced metabolic disorders, particularly obesity, insulin resistance, dyslipidemia, and hypertension, may be inherited through epigenetic pathways.

RESULTS: The evidence analyzed suggests that the gut microbiota serves as a diverse metabolic and immunological organ. Its disruption affects the production of short-chain fatty acids, bile acid metabolism, immune signaling, and the redox balance, which contributes to the development of obesity, insulin resistance, and metabolic syndrome.

CONCLUSIONS: This review highlights key epigenetic mechanisms underlying metabolic disorders and oxidative stress in the context of gut dysbiosis. Furthermore, therapeutic strategies targeting the gut microbiota, such as dietary interventions, prebiotics, probiotics, postbiotics, and fecal microbiota transplantation, hold promise for mitigating oxidative stress and inflammation associated with metabolic syndrome.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Dysbiosis/microbiology/metabolism
Oxidative Stress
*Metabolic Diseases/microbiology/metabolism
Epigenesis, Genetic
Probiotics
Inflammation/microbiology
Animals

@article {pmid41901066,
year = {2026},
author = {Thomas, EG and Ortutu, BF and Watson, JC and Ong, E and Blankley, KE and Meaurio Martin, A and Shankar, S and Zhang, D and Boland, DJ and Wu, CS},
title = {Purified Diets Lacking Fermentable Fiber Reduce Microbial Diversity, Alter Epithelial Transcriptome, and Exacerbate Colitis.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901066},
issn = {2072-6643},
support = {R21ES036683/ES/NIEHS NIH HHS/United States ; RP230204//Texas A&M Health-Center of Excellence in Cancer Research/ ; 58-3091-1-018//Texas A&M AgriLife Institute for Advancing Health Through Agriculture/ ; },
mesh = {Animals ; *Dietary Fiber/administration & dosage ; Mice, Inbred C57BL ; Male ; *Gastrointestinal Microbiome ; *Transcriptome ; *Colitis/microbiology/chemically induced ; Mice ; *Intestinal Mucosa/metabolism/microbiology ; Fermentation ; Fatty Acids, Volatile/metabolism ; Colon/metabolism/microbiology ; Dextran Sulfate ; Feces/microbiology ; *Diet ; Disease Models, Animal ; },
abstract = {Background/Objectives: Dietary fibers play key roles in shaping gut microbiome and intestinal homeostasis. While purified diets offer experimental precision and reproducibility in rodent models, they omit the complex mixture of fermentable and non-fermentable fibers found in grain-based chow diets. We hypothesized that excluding fermentable fiber impairs intestinal homeostasis by reducing microbial metabolites and altering the colonic epithelial transcriptome, thereby increasing susceptibility to inflammation. Methods: Wildtype male C57BL/6 mice were maintained on either a standard grain-based chow diet or a purified low-fat diet (LFD) containing 5% non-fermentable cellulose for ten weeks. Fecal microbiomes, short-chain fatty acid (SCFA) profiles, and colonic epithelial transcriptomes were analyzed. A separate group was challenged with dextran sodium sulfate (DSS) following a five-week dietary intervention to compare colitis severity between the two diet groups. Results: Relative to mice fed the grain-based chow, those consuming the purified LFD (containing only non-fermentable cellulose) showed decreased gut microbial diversity and significantly lower SCFA levels. These changes were accompanied by marked differences in colonic epithelial cell transcriptomes. In LFD-fed mice, the top upregulated gene networks included ribosomal pathways and MHC complex protein binding, suggesting increased growth and gut inflammation. The most downregulated pathways included mineral absorption, actin and tubulin binding, and membrane organelle assembly, indicating major alterations in cellular structure and transport. LFD-fed mice also exhibited increased colonic expression of S100a9, a gut inflammation biomarker, and more severe disease symptoms when challenged with DSS compared to chow-fed mice. Conclusions: Fermentable fibers are one of the factors contributing to intestinal homeostasis and mitigating the severity of ulcerative colitis.},
}

Animals
*Dietary Fiber/administration & dosage
Mice, Inbred C57BL
Male
*Gastrointestinal Microbiome
*Transcriptome
*Colitis/microbiology/chemically induced
Mice
*Intestinal Mucosa/metabolism/microbiology
Fermentation
Fatty Acids, Volatile/metabolism
Colon/metabolism/microbiology
Dextran Sulfate
Feces/microbiology
*Diet
Disease Models, Animal

@article {pmid41901079,
year = {2026},
author = {Cirio, S and Mantegazza, G and Salerno, C and Guglielmetti, S and Allam, A and Campus, G and Cagetti, MG},
title = {Assessing the Impact of Heyndrickxia coagulans Administered Through Sugar-Free Chewing Gum on Dental Biofilm: A Double-Blind Randomized Controlled Trial.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901079},
issn = {2072-6643},
mesh = {Humans ; *Chewing Gum ; Double-Blind Method ; *Biofilms/drug effects ; Male ; Female ; Adult ; *Dental Plaque/microbiology ; *Probiotics/administration & dosage ; Middle Aged ; Young Adult ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Background:Heyndrickxia coagulans has emerged as a candidate for oral health applications, and chewing gum offers a promising delivery method. This study evaluates whether H. coagulans delivered via sugar-free chewing gum can induce detectable changes in plaque microbial ecology. Methods: A randomized, double-blind, placebo-controlled clinical trial was conducted on 52 healthy adults. Participants consumed probiotic or control gum for 4 weeks. Dental plaque was collected at baseline (T0), mid-intervention (T1), end of intervention (T2), and one week post-intervention (T3). qPCR quantified H. coagulans, while 16S rRNA gene profiling assessed microbial diversity and taxonomic composition. Statistical analyses included rank-based difference-in-differences models, Wilcoxon and Mann-Whitney tests, and differential abundance inference based on negative binomial modeling. Results: Forty-four subjects completed the study. In the Intervention group, the strain was detected in 71.4% of participants at T1 and 61.9% at T2, and it persisted in 9.5% at T3. Differential abundance analysis revealed a broad depletion of taxa linked to oral dysbiosis at T2 with partial persistence at T3, along with selective enrichment of beneficial strains. Conclusions:H. coagulans delivered via chewing gum can reach the dental biofilm and induce modest, transient shifts in microbial composition. However, these biofilm ecology findings should be interpreted in the context of clinical outcomes.},
}

Humans
*Chewing Gum
Double-Blind Method
*Biofilms/drug effects
Male
Female
Adult
*Dental Plaque/microbiology
*Probiotics/administration & dosage
Middle Aged
Young Adult
RNA, Ribosomal, 16S/genetics

@article {pmid41901112,
year = {2026},
author = {Solano-Aguilar, G and Lakshman, S and Chen, C and Beshah, E and Molokin, A and Vinyard, B and Dawson, HD and Santin-Duran, M and Bruna, G and Smith, A and Urban, JF},
title = {Fruit and Vegetable Supplemented-Diet Ameliorates Dextran Sodium Sulfate (DSS)-Induced Colitis by Modulating Host Transcriptome and Gut Metagenome Response.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901112},
issn = {2072-6643},
support = {Cris 8040-51000-058-00D//United States Department of Agriculture/ ; },
mesh = {Animals ; Dextran Sulfate ; *Fruit ; *Colitis/chemically induced/prevention & control/microbiology/diet therapy ; *Transcriptome ; *Gastrointestinal Microbiome ; *Dietary Supplements ; *Vegetables ; Swine ; *Metagenome ; Disease Models, Animal ; *Diet ; Colon/pathology ; },
abstract = {Background/Objectives: Dietary intake of fruits and vegetables (FVs) has been inversely associated with a lower risk of ulcerative colitis. Using a pig model, we evaluated the effect of FV supplementation on dextran sulfate sodium (DSS)-induced colitis. Methods: Six-week-old pigs were fed a grower diet (negative control), grower diet + 4% DSS (positive control), half-FV diet + DSS, or full-FV diet + DSS. FV levels matched half or full daily recommendations from the Dietary Guidelines for Americans (DGA). Clinical signs were monitored; proximal colon contents (PCs) and mucosa (PCM) were analyzed for metagenome, transcriptome and histopathology. Results: Full-FV pigs showed no diarrhea, less fecal occult blood (FOB), crypt hyperplasia, but no changes in gene expression or microbiome diversity (p < 0.05). Half-FV pigs had increased FOB, differentially expressed genes (DEGs) linked to tissue remodeling, crypt/goblet cell hyperplasia and two cases of diarrhea (p < 0.05). DSS controls showed reduced immune-related DEGs, altered microbiome, PCM erosion, FOB, and persistent diarrhea in one pig (p < 0.05). Conclusions: A three-week full-FV diet conferred protection against DSS-induced colitis, with a dose-dependent protection of intestinal tissue and gut metagenome under inflammatory challenge.},
}

Animals
Dextran Sulfate
*Fruit
*Colitis/chemically induced/prevention & control/microbiology/diet therapy
*Transcriptome
*Gastrointestinal Microbiome
*Dietary Supplements
*Vegetables
Swine
*Metagenome
Disease Models, Animal
*Diet
Colon/pathology

@article {pmid41901128,
year = {2026},
author = {Lupu, VV and Nedelcu, AH and Borka-Balas, R and Anton, CR and Tarnita, I and Azoicai, A and Forna, L and Munteanu, D and Anton, SC and Shawais, SK and Badescu, MC and Salaru, DL and Morariu, ID and Anton, E and Petrariu, F and Lupu, A},
title = {The Gut Microbiota: An Essential Component in Understanding Pediatric Obesity: A Narrative Review.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901128},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Pediatric Obesity/microbiology ; Child ; Dysbiosis/microbiology ; Probiotics ; },
abstract = {Background: Childhood obesity has become a major public health concern worldwide. Increasing evidence suggests that alterations in the gut microbiome may play a significant role in the development and progression of pediatric obesity. This narrative review synthesizes and analyzes recent studies investigating microbiome alterations in children with obesity, highlighting emerging insights and their potential implications for disease management. Understanding the relationship between gut microbial composition and obesity may provide new perspectives for prevention and therapeutic strategies in overweight pediatric populations. This narrative review was conducted through a search of major biomedical databases, including PubMed and Web of Science, complemented by manual screening of reference lists of relevant articles. Key findings: Children affected by obesity exhibit significant changes in gut microbiome composition, characterized by reduced microbial diversity and predominance of the Firmicutes and Bacteroidetes phyla. The balance between these two bacterial groups appears critical for maintaining gut homeostasis. Studies consistently report an increased Firmicutes-to-Bacteroidetes ratio in children with elevated body weight, suggesting that disruption of this balance may contribute to metabolic dysregulation and obesity-related pathologies. Given the essential role of the gut microbiota in nutrient metabolism and energy extraction, dysbiosis in obesity is associated with enhanced energy harvest and lipid absorption. Certain bacterial populations may promote increased caloric uptake, thereby contributing to weight gain and adiposity. Multidimensional interventions, including dietary modification and physical activity, have demonstrated the potential to reduce obesogenic microbiota patterns and restore microbial diversity. Additionally, probiotic supplementation is being investigated as a strategy to reestablish microbial homeostasis and potentially support body mass index reduction. Despite promising findings, further research is required to clarify mechanisms, establish causality, and determine the clinical effectiveness of microbiome-targeted therapies before they can be fully integrated into the management of pediatric obesity.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Pediatric Obesity/microbiology
Child
Dysbiosis/microbiology
Probiotics

@article {pmid41901151,
year = {2026},
author = {Green, GBH and Cox-Holmes, AN and Flowers, JT and Williams, MB and Potier, ACE and Brandom, JL and Watts, SA and Luke, R and Yu, JS and McFarland, BC},
title = {Dietary and Nutritional Strategies for Patients with Glioma: A Narrative Review of Treatment, Recovery, Immune Support, and Microbiota Modulation.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901151},
issn = {2072-6643},
support = {R01CA270750-01A1/CA/NCI NIH HHS/United States ; T32NS121721/NS/NINDS NIH HHS/United States ; },
mesh = {Humans ; *Glioma/therapy/immunology/microbiology/diet therapy ; *Gastrointestinal Microbiome ; *Brain Neoplasms/therapy/immunology/microbiology/diet therapy ; *Nutritional Support/methods ; Quality of Life ; *Diet ; Tumor Microenvironment ; Nutritional Status ; },
abstract = {This narrative review aims to explore the relationship between glioma and nutrition throughout stages of treatment and recovery. Gliomas are aggressive brain tumors that significantly impair quality of life and present treatment challenges. There has been a growing interest regarding the gut-brain axis and the microbiome, particularly their roles in modulating immune function and influencing the response to cancer treatment. This review examines how specific nutritional approaches may assist patients throughout the course of chemotherapy, radiation, immunotherapy, surgical intervention, and the recovery process. It also addresses the potential for integrative nutritional approaches to complement conventional treatment and improve clinical outcomes. Emerging evidence suggests that nutrition may influence immune function, treatment-related side effects, and the tumor microenvironment, in part through effects on the gut microbiota. Nutritional support during therapy has been linked to increased strength, decreased inflammation, and improved treatment tolerance. Dietary patterns may influence gut-brain interactions and systemic immune responses, opening the potential to improve therapeutic outcomes in glioma. In summary, nutrition may represent an important supportive component of glioma care, while microbiota-mediated and metabolic dietary strategies remain areas of active investigation. Further clinical studies are needed to determine whether specific nutritional interventions can improve survival, treatment response, or quality of life in patients with glioma.},
}

Humans
*Glioma/therapy/immunology/microbiology/diet therapy
*Gastrointestinal Microbiome
*Brain Neoplasms/therapy/immunology/microbiology/diet therapy
*Nutritional Support/methods
Quality of Life
*Diet
Tumor Microenvironment
Nutritional Status

@article {pmid41901159,
year = {2026},
author = {Brăgaru, MA and Kraft, A and Moldovan, CA and Moldovan, AD and Răzvan, A and Cochior, D and Luca, A and Nica-Badea, D and Chirsanov Capanu, ȘE and Rusu, E},
title = {Optimizing Perioperative Nutrition in Elective Gastrointestinal Surgery: An ERAS-Focused Narrative Review.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901159},
issn = {2072-6643},
mesh = {Humans ; *Elective Surgical Procedures/adverse effects ; *Digestive System Surgical Procedures/adverse effects ; *Perioperative Care/methods ; *Malnutrition/prevention & control ; Postoperative Complications/prevention & control ; *Enhanced Recovery After Surgery ; Sarcopenia/prevention & control ; *Nutritional Support/methods ; Nutritional Status ; Dietary Supplements ; },
abstract = {Background/Objectives: Perioperative malnutrition, sarcopenia, and reduced functional reserve are frequent in adults undergoing elective gastrointestinal (GI) surgery and are associated with higher postoperative morbidity and delayed recovery. Enhanced Recovery After Surgery (ERAS) pathways incorporate nutrition-focused elements, but reported effects vary across procedures, protocols, and baseline risk. This review aims to summarize and critically appraise current evidence on perioperative nutritional strategies within ERAS-focused elective GI care, including risk identification, nutritional prehabilitation (oral nutritional supplements and immunonutrition), preoperative carbohydrate loading, early postoperative feeding, and selected microbiome-directed adjuncts. Methods: This narrative literature review was informed by a focused search of PubMed/MEDLINE and Scopus (2010-early 2026), supplemented by targeted screening of relevant clinical practice guidelines and consensus statements (e.g., ESPEN). Evidence was interpreted by hierarchy (guidelines/meta-analyses, randomized trials, observational studies) and discussed with attention to heterogeneity in surgical populations, intervention definitions (composition, timing, duration), and endpoint reporting. Results: Early nutritional risk screening is consistently supported to identify malnutrition and sarcopenia and to trigger tailored optimization plans. Perioperative oral nutritional supplementation, particularly when started preoperatively and continued postoperatively, is frequently associated with improved intake and reduced infectious morbidity in malnourished or at-risk patients, though effect sizes vary. Immunonutrition shows potential benefit in selected high-risk settings but remains formulation- and timing-dependent. Carbohydrate loading is generally endorsed within ERAS and may reduce insulin resistance and improve patient comfort, while impacts on major clinical outcomes are context-dependent. Early oral/enteral feeding is feasible in many elective GI procedures and may accelerate gastrointestinal recovery without increasing major complications when implemented with structured advancement and appropriate patient selection. Probiotics/synbiotics show the most consistent signals in colorectal surgery, with strain-specific effects and important safety boundaries in immunocompromised or critically ill patients. Conclusions: Perioperative nutritional optimization is a core component of elective GI surgical care within ERAS pathways. Benefits are most reproducible in higher-risk patients and when interventions are integrated into high-compliance multidisciplinary programs. Future research should prioritize procedure-specific, risk-stratified trials with standardized interventions and clinically meaningful endpoints.},
}

Humans
*Elective Surgical Procedures/adverse effects
*Digestive System Surgical Procedures/adverse effects
*Perioperative Care/methods
*Malnutrition/prevention & control
Postoperative Complications/prevention & control
*Enhanced Recovery After Surgery
Sarcopenia/prevention & control
*Nutritional Support/methods
Nutritional Status
Dietary Supplements

@article {pmid41901182,
year = {2026},
author = {Silverstein, HR and Rizvanov, AA and Haines, DD and Mahmoud, FF and Rose, SC and Solovyeva, VV and Kitaeva, KV and Tosaki, A},
title = {The Simultaneous Prevention of Multiple Diseases: A "One Ring to Rule Them All" Framework for Redox-Driven Health and Longevity.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901182},
issn = {2072-6643},
support = {A.A.R., V.V.S. and K.V.K. were supported by the Kazan Federal University Strategic Academic Leadership Program (PRIORITY-2030)//Ministry of Science and Higher Education of the Russian Federation/ ; This study was also supported by the HUN-REN-DE//Hungarian Research Network/ ; },
mesh = {Humans ; Oxidation-Reduction ; *Longevity ; Oxidative Stress ; Antioxidants ; Dietary Supplements ; *Noncommunicable Diseases/prevention & control ; Cardiovascular Diseases/prevention & control ; Diet ; },
abstract = {Chronic non-communicable diseases rarely occur in isolation; cardiovascular, metabolic, neurodegenerative, malignant, and age-associated disorders share upstream drivers including oxidative stress, chronic inflammation, mitochondrial dysfunction, and metabolic imbalance. This narrative review synthesizes epidemiological, interventional, and mechanistic studies identified through targeted literature searches to examine redox biology as a shared mechanistic hub linking these conditions. We evaluate antioxidant-rich dietary patterns, selected nutraceuticals, myocardial ischemia-reperfusion injury as a clinical exemplar, rare redox-imbalance disorders as mechanistic stress models, and emerging gene-based reinforcement of endogenous antioxidant systems. Rather than proposing clinical targets, we present an integrative, hypothesis-generating framework illustrating how coordinated lifestyle-driven modulation of redox balance may simultaneously influence multiple disease trajectories. Collectively, the evidence supports a unified redox framework for multi-disease prevention for multi-disease prevention and future intervention design.},
}

Humans
Oxidation-Reduction
*Longevity
Oxidative Stress
Antioxidants
Dietary Supplements
*Noncommunicable Diseases/prevention & control
Cardiovascular Diseases/prevention & control
Diet

@article {pmid41901189,
year = {2026},
author = {Witt, BL and Singaravelan, N and Tollefsbol, TO},
title = {Combined Effects of Withaferin A and Sodium Butyrate on NF-κB Signaling and Epigenetic Regulation in Breast Cancer Cells.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901189},
issn = {2072-6643},
support = {R01CA178441//Natrional Institutes of Health/ ; },
mesh = {Humans ; *Withanolides/pharmacology ; *Epigenesis, Genetic/drug effects ; *Signal Transduction/drug effects ; Female ; *Butyric Acid/pharmacology ; *NF-kappa B/metabolism/genetics ; Cell Line, Tumor ; *Breast Neoplasms/genetics/drug therapy/metabolism ; Cell Survival/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; MCF-7 Cells ; Triple Negative Breast Neoplasms/drug therapy/genetics ; },
abstract = {Background/Objectives: There is a clear need for more options to control the progression of breast cancer and prevent the occurrence of breast cancer in minority populations that have a higher rate of mortality due to triple-negative breast cancer (TNBC) subtypes. Prevalent nutraceuticals such as Ashwagandha (also known as the Indian Winter Cherry) have anti-inflammatory and apoptotic capabilities, as well as the ability to inhibit cancer growth. The purpose of this study is to analyze the novel combination of withaferin A (derived from the Indian Winter Cherry and known to have histone deacetylase inhibition capabilities) and sodium butyrate (a short-chain fatty acid produced from the gut microbiome and known to have DNA methyltransferase inhibition capabilities) treatment on breast cancer-derived cell lines. There is a scientific gap of possible causality of decreasing breast cancer progression when treated with sodium butyrate and withaferin A. Methods: Two in vitro cell viability assays were utilized consisting of [MTT (4,5 Dimethylthiazol-2-yl)] and the neutral red assay to analyze the impact of treatment of compounds alone and in combination on breast cancer cells for 72 h. The Highest Single Agent (HSA) combination analysis was utilized to derive combination indexes for our breast cancer cell types. Protein and gene expression was investigated for Class 1 histone deacetylases, de novo DNA methyltransferase, the p65 subunit of NF-κB, and NFκB1. Lastly, DNA methyltransferase enzymatic activity was analyzed via the Epigentek DNMT Activity/Inhibition ELISA Easy Kit. Results: Through the cell viability assay [MTT (4,5 Dimethylthiazol-2-yl)], MCF-7, MDA-MB-231, and MDA-MB-157 cells were found to have a decrease in cell viability due to combinatorial treatment with withaferin A and sodium butyrate. Western blot results depicted a decrease in protein expression levels for DNA methyltransferases due to the administration of 2.5 mM sodium butyrate and 0.2 µM withaferin A alone and in combination for breast cancer cell lines MCF-7, MDA-MB-231, and MDA-MB-157. Additionally, the combination of these two components have successfully inhibited the progression of the NFκB1 gene within analysis through the quantitative polymerase chain reaction (qPCR). Conclusions: The novel combination of withaferin A and sodium butyrate have markedly reduced the progression of breast cancer-derived cell lines for cell viability, epigenetic DNMT gene expression, as well as inhibiting NFκB1 signaling on the gene expression level.},
}

Humans
*Withanolides/pharmacology
*Epigenesis, Genetic/drug effects
*Signal Transduction/drug effects
Female
*Butyric Acid/pharmacology
*NF-kappa B/metabolism/genetics
Cell Line, Tumor
*Breast Neoplasms/genetics/drug therapy/metabolism
Cell Survival/drug effects
Gene Expression Regulation, Neoplastic/drug effects
MCF-7 Cells
Triple Negative Breast Neoplasms/drug therapy/genetics

@article {pmid41901191,
year = {2026},
author = {Di Maio, G and Tafuri, MG and Casillo, M and Messina, A and Allocca, S and Villano, I and Moscatelli, F and Monda, A and La Marra, M and Monda, V},
title = {Physiological Regulation of Nutritional and Metabolic Biomarkers in Obesity: Implications for Precision Nutrition.},
journal = {Nutrients},
volume = {18},
number = {6},
pages = {},
pmid = {41901191},
issn = {2072-6643},
mesh = {Humans ; *Biomarkers/blood/metabolism ; *Obesity/metabolism/physiopathology ; *Precision Medicine ; *Nutritional Status ; Adipokines/blood ; Gastrointestinal Microbiome ; Insulin Resistance ; },
abstract = {Obesity represents a heterogeneous metabolic disorder characterized by substantial interindividual variation in inflammatory status, insulin sensitivity, and cardiometabolic risk. Traditional anthropometric measures fail to capture this metabolic diversity, limiting risk stratification and personalized intervention strategies. This review critically examines nutritional and metabolic biomarkers that reflect the physiological dysregulation underlying obesity, including adipokines (leptin, adiponectin, resistin), inflammatory markers (C-reactive protein, interleukin-6, TNF-α), insulin resistance indices (HOMA-IR, fasting insulin, HbA1c), and lipid metabolism indicators (LDL cholesterol, triglycerides, HDL cholesterol, and liver enzymes such as ALT and GGT). Among these, elevated CRP, reduced adiponectin, and increased HOMA-IR have demonstrated the strongest clinical utility for early metabolic risk identification. We further evaluate emerging biomarkers-including circulating microRNAs, gut microbiota-derived metabolites (short-chain fatty acids, TMAO, lipopolysaccharides), and bile acid profiles-which offer additional mechanistic insight into diet-microbiome-host interactions. We systematically assess the mechanistic basis, clinical relevance, and nutritional modulation of each biomarker class, emphasizing how dietary composition-particularly fatty acid quality, fiber intake, and overall dietary patterns such as the Mediterranean diet-influences biomarker profiles and metabolic outcomes. Furthermore, we explore how biomarker-based phenotyping enables precision nutrition approaches by identifying individuals most likely to benefit from specific dietary interventions. Integration of multi-biomarker panels with clinical and genetic data holds promise for advancing from population-based dietary guidelines toward individualized nutrition strategies that optimize metabolic health and prevent obesity-related complications. Future research should prioritize validating biomarker-guided intervention frameworks, establishing standardized thresholds across diverse populations, and developing clinically implementable tools for personalized nutritional medicine.},
}

Humans
*Biomarkers/blood/metabolism
*Obesity/metabolism/physiopathology
*Precision Medicine
*Nutritional Status
Adipokines/blood
Gastrointestinal Microbiome
Insulin Resistance

@article {pmid41901195,
year = {2026},
author = {Xiong, H and Ji, S and Ding, Q and Zhou, Y and Yao, X and Zhu, Y},
title = {The Impact of Seasonal and Meteorological Factors on Microorganisms Present in Knee Joint Effusions Among Patients with Rheumatoid Arthritis.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {19},
number = {3},
pages = {},
pmid = {41901195},
issn = {1424-8247},
support = {the Macau Science and Technology Development Fund (FDCT (0012/2021/AMJ, 003/2022/ALC,0092/2022/A2, 0144/2022/A3)).The National Natural Science Foundation of China (No. 81973320,No.82160869). Shenzhen-HongKong-Macao Science and Technology Fund (Category C://the Macau Science and Technology Development Fund、The National Natural Science Foundation of China、Shenzhen-HongKong-Macao Science and Technology Fund、University Joint Laboratory of Guangdong Province and Macao Region on Molecular Targets and Intervention/ ; },
abstract = {Background/Objectives: Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent synovial inflammation and vascular abnormalities. Emerging evidence suggests that dysbiosis of the microbiome contributes to the pathogenesis of this disease, while seasonal and meteorological variations represent significant factors influencing microbial community dynamics. However, the specific pathological mechanisms mediated by microbial populations within knee joint effusions of RA patients remain poorly elucidated. The present study employs 16S rRNA high-throughput sequencing technology to characterize seasonal variation patterns affecting microbial communities in knee joint effusions of RA patients and to investigate the relationship between microbial community structures and climatic lag effects. Methods: Microbial communities in knee joint effusion samples obtained from RA patients were analyzed using 16S rRNA high-throughput sequencing methodologies. A Distributed Lag Non-linear Model (DLNM) was applied to quantify the delayed effects of climatic variables on microbial community composition. The correlation patterns between meteorological parameters and community structure were elucidated through the integration of ridge regression and redundancy analysis (RDA). Preliminary identification of potential biomarkers was conducted using random forest algorithms. Results: According to research findings, the microbial composition of knee joint effusions in RA patients shows seasonal fluctuation patterns that are compatible with those seen in RA patients, even though there is no discernible seasonal change in β-diversity. Compared with samples obtained during other seasons, spring specimens exhibited significantly elevated relative abundances of both beneficial microorganisms and opportunistic pathogenic taxa. Random forest modeling identified Escherichia-Shigella and Curtobacterium as preliminary candidate biomarkers; however, external validation is required to establish their specificity as disease indicators. Further analysis revealed that although short-term meteorological fluctuations exert minimal influence on overall microbial diversity, specific alterations in mean wind speed (MWS) and relative humidity (RH) drive compositional changes in the microbial community, manifested as rapid responses from dominant bacterial taxa and compensatory buffering effects from rare taxa. Conclusions: This study suggests that the synovial cavity microbiota in RA patients may exhibit seasonal variation patterns that are statistically associated with environmental parameters, particularly humidity and temperature. Due to the inherent limitations of the cross-sectional study design, the preliminary candidate biomarkers identified herein require validation through external cohorts. Additional investigations incorporating healthy controls and osteoarthritis (OA) cohorts are necessary to confirm specificity and to elucidate the therapeutic potential of these microbial targets for RA microbiome interventions. Currently, insufficient evidence exists to establish causal relationships among microbial populations, joint pathology, and climatic factors. Longitudinal cohort studies are imperative to validate the temporal dynamics and clinical significance of these associations.},
}

@article {pmid41901248,
year = {2026},
author = {Xue, X and Zhang, F and Wang, H and Guo, M and Qin, W and Yang, Y and Huo, Z and Li, X and Han, Q and Li, X},
title = {Si-Wu-Tang Targets Microbiota Homeostasis and Intestinal Mucosal Barriers to Provide Protection Against MASLD by Favoring P. goldsteinii-like Taxa Colonization.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {19},
number = {3},
pages = {},
pmid = {41901248},
issn = {1424-8247},
support = {ZYGXQNJSKYCXNLZCXM-H4//Scientific Research Innovation Capability Support Project for Young Faculty/ ; 2022YFC3502100//National Key Research and Development Program on Modernization of Traditional Chinese Medicine/ ; 2023-JYB-JBZD-046//Fundamental Research Funds for the Central Universities/ ; },
abstract = {Objective: This study examined the pharmacological mechanisms of the therapeutic benefits of SWT to MASLD via regulating the gut-liver axis. Methods: The components of SWT were analyzed by liquid chromatograph mass spectrometer (LC-MS). After establishing an MCD-induced MASLD mice model, we invested the protective mechanism of SWT through 16S rRNA sequencing combined with molecular biological experiments. After eliminating the intestinal microbiota through an antibiotic cocktail experiment, we identified the key microbiota by which SWT improves MASLD. Results: SWT markedly reduced MASLD injury by alleviating intestinal inflammation and restoring the intestinal mucosal barrier, which could be reversed following alcohol exposure. Additionally, SWT altered the intestinal flora of MASLD mice, significantly raising the relative abundance of Parabacteroides goldsteinii-like taxa, while alcohol caused the destruction of P. goldsteinii-like-taxa-centered probiotic habitats and a proliferation of pathogenic bacteria, especially Bacteroides intestinalis-like taxa. After the elimination of intestinal flora, the anti-MASLD effect of SWT was lost. Moreover, the supplement of P. goldsteinii could significantly ameliorate liver damage caused by an MCD diet, functioning similarly to SWT. However, the liver-protective effect of SWT was suppressed following the administration of B. intestinalis. Conclusions: SWT ameliorates MCD diet-induced MASLD via modulating intestinal microbiota homeostasis and restoring intestinal mucosal barriers. Given that P. goldsteinii is effective for treating MASLD, it provides insights into new therapeutic strategies.},
}

@article {pmid41901456,
year = {2026},
author = {Tian, S and Zhang, N and Lin, G and Cheng, X and Wang, F and Chang, P and Ahammed, GJ and Shi, Q and Nie, WF and Zhang, Y},
title = {Epigenetic Regulation of Root-Associated Microbiota: Mechanisms and Horticultural Applications.},
journal = {Plants (Basel, Switzerland)},
volume = {15},
number = {6},
pages = {},
pmid = {41901456},
issn = {2223-7747},
abstract = {The dynamic interaction between plants and their root-associated microbiota represents a sophisticated and profound biological communication that regulates plant development and the formation of adaptation to the surrounding environment. These interactions function as critical regulators of multiple physiological processes, finally influencing soil fertility and agricultural productivity. Plants have evolved epigenetic networks that regulate beneficial plant-microbe interactions through regulating immune responses, gene regulation, and metabolite production to enhance stress tolerance and soil adaptation. These regulations collectively govern microbial colonization patterns while establishing reciprocal feedback loops through root exudate-microbe interactions. This review systematically updates contemporary advances in understanding how epigenetic modifications shape rhizosphere microbiome composition and function, and discusses their potential applications in enhancing the yield and quality of horticultural crops, as well as in mitigating continuous cropping obstacles.},
}

@article {pmid41901493,
year = {2026},
author = {Curci, LM and Carrozzo, S and Pecatelli, G and Semeraro, T and Tafuro, C and Lenucci, MS and De Caroli, M},
title = {Environmental and Cultivation Effects on Growth and Phytochemical Profiles of Chicory (Cichorium intybus L.) in Soil, Hydroponics, and Aquaponics.},
journal = {Plants (Basel, Switzerland)},
volume = {15},
number = {6},
pages = {},
pmid = {41901493},
issn = {2223-7747},
abstract = {The increasing demand for sustainable food production has intensified interest in controlled-environment agriculture and soilless cultivation systems. This study evaluated the performance of local chicory (Cichorium intybus L., cultivar "Otrantina") grown for 45 days in soil, hydroponics, and decoupled aquaponics under two different environments: a fully controlled growth chamber and a naturally variable greenhouse. Morphological, anatomical, biochemical, and physiological traits were analyzed to assess the combined influence of growth environment and cultivation system on plant development and nutritional quality. Across all parameters, the growth environment emerged as the main driver of plant performance. Greenhouse-grown plants exhibited greater leaf expansion, enhanced mesophyll and vascular development, and higher fresh and dry biomass than those cultivated in the growth chamber. Within each environment, hydroponics consistently supported vigorous growth, whereas aquaponics produced smaller leaves and pronounced root elongation, likely reflecting nutrient and pH instability in the decoupled system. Biochemical analyses revealed system-specific adaptive responses. Soilless cultivation promoted higher lipid accumulation and, under growth chamber conditions, increased protein content. Aquaponically grown plants, particularly in the greenhouse, accumulated elevated levels of soluble sugars and phenolic antioxidants, consistent with stress-related metabolic activation. In contrast, soil-grown plants displayed the highest flavonoid concentrations, suggesting a prominent role of rhizosphere-microbiome interactions in modulating secondary metabolism. Overall, these results indicate that, under the tested conditions, environmental control exerts a stronger influence than cultivation systems on chicory growth and metabolism. Hydroponics proved to be the most efficient system for biomass production, whereas aquaponics requires improved nutrient management to ensure stable growth and quality. The distinct metabolic profiles associated with each cultivation system highlight opportunities to tailor chicory nutraceutical traits within sustainable controlled-environment agriculture.},
}

@article {pmid41901497,
year = {2026},
author = {Liang, A and Wang, F and Liu, T and Liao, Y and Mu, Z},
title = {Habitat Filtering Shapes Root Endophytic Microbiome Assembly and Its Association with Fruit Quality in Lycium ruthenicum from the Tarim Basin.},
journal = {Plants (Basel, Switzerland)},
volume = {15},
number = {6},
pages = {},
pmid = {41901497},
issn = {2223-7747},
support = {no. 32160390//the National Natural Science Foundation of China/ ; no. 524307001//the Tianchi Talents-Innovative Leaders of Xinjiang/ ; no. TDZKBS202206//the President's Fund of Tarim University/ ; },
abstract = {Lycium ruthenicum is a typical desert halophyte with strong stress resistance and high medicinal value in the Tarim Basin. Root endophytic microbes play critical roles in host adaptation, nutrient cycling, and secondary metabolite accumulation. To clarify the diversity patterns of root endophytic bacteria and fungi and their relationships with environmental factors and fruit quality, high-throughput sequencing was used to analyze microbial community characteristics of Lycium ruthenicum collected from different habitats in the Tarim Basin. The results showed that rarefaction curves of alpha diversity indices (Chao1, Shannon, Pielou_e) tended to be saturated, indicating sufficient sequencing depth. Principal coordinate analysis (PCoA) revealed significant habitat-driven differentiation in both bacterial and fungal community structures. Community composition analysis showed that the relative abundance of dominant taxa at the phylum and genus levels differed significantly among sampling sites. Co-occurrence network analysis indicated that bacterial and fungal networks exhibited high modularity and were dominated by positive synergistic interactions, with Pseudomonas, Bacillus, Sphingomonas, Alternaria, and Fusarium as key hub genera. Moreover, root endophytic communities were significantly correlated with climatic variables, soil physicochemical properties, and fruit quality traits, including anthocyanin (AC), proanthocyanidin (PA), total flavonoids (TF), and total polyphenols (TP). Several keystone microbial genera were closely associated with the accumulation of functional metabolites in fruits. This study reveals the biogeographic distribution and co-occurrence characteristics of root endophytes in Lycium ruthenicum and provides a theoretical basis for understanding microbe-host-environment interactions and the quality improvement of desert medicinal plants.},
}

@article {pmid41901529,
year = {2026},
author = {Bečić, T and Jukić, I and Prižmić, PŠ and Matulić, I and Đogaš, H and Radić, M and Radić, J and Vuković, J and Fabijanić, D},
title = {Heart-Gut Axis in Cardiometabolic Disease: Microbiome-Mediated Pathways Linking Metabolic Syndrome to Cardiovascular Risk.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {62},
number = {3},
pages = {},
pmid = {41901529},
issn = {1648-9144},
mesh = {Humans ; *Metabolic Syndrome/complications/physiopathology/microbiology ; *Gastrointestinal Microbiome/physiology ; *Cardiovascular Diseases/physiopathology/etiology/microbiology ; Dysbiosis/complications ; Cardiometabolic Risk Factors ; },
abstract = {Background and Objectives: Cardiometabolic disease, a term encompassing metabolic syndrome (MS) and cardiovascular disease (CVD), represents a major and growing global health burden driven by interconnected metabolic and cardiovascular dysfunction. Emerging evidence suggests that the gut microbiota plays a central role in modulating metabolic, inflammatory, and cardiovascular (CV) pathways, giving rise to the concept of the heart-gut axis. However, human evidence integrating microbiome-mediated mechanisms across the cardiometabolic spectrum remains incompletely synthesized. This focused systematic review aimed to synthesize the current human evidence on microbiome-mediated mechanisms linking metabolic syndrome (MS) and related metabolic phenotypes with cardiovascular risk (CVR) and subclinical cardiovascular (CV) outcomes within the conceptual framework of the heart-gut axis. Materials and Methods: A systematic literature search was conducted in PubMed, Scopus, Web of Science, and the Cochrane Library in accordance with PRISMA 2020 guidelines. Human observational and interventional studies evaluating gut microbiota composition, function, or microbiota-derived metabolites in relation to cardiometabolic, and CV outcomes were included. Risk of bias was assessed using the Cochrane RoB 2 and ROBINS-I tools, and findings were synthesized narratively. Results: Ten human studies published between 2016 and 2025 met the inclusion criteria. Across these studies, gut dysbiosis was consistently associated with adverse cardiometabolic risk profiles and subclinical CV outcomes, including insulin resistance, systemic inflammation, subclinical atherosclerosis, and CV prognosis in high-risk populations. Microbiota-derived metabolites, particularly trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), as well as emerging metabolites such as phenylacetylglutamine (PAGln) and imidazole propionate (ImP), were identified as key mediators linking metabolic syndrome and related metabolic disturbances with CVR and subclinical cardiovascular disease (CVD). Markers of intestinal barrier dysfunction and endotoxemia further supported the role of chronic low-grade inflammation within the heart-gut axis. Conclusions: Current human evidence supports the heart-gut axis as a biologically plausible and clinically relevant contributor to cardiometabolic disease. Gut microbiota-derived metabolites, intestinal barrier dysfunction, and systemic inflammation represent interconnected pathways linking MS with CVR. Advancing our understanding of these mechanisms may inform the development of microbiome-targeted strategies to complement established approaches for cardiometabolic and CV prevention.},
}

Humans
*Metabolic Syndrome/complications/physiopathology/microbiology
*Gastrointestinal Microbiome/physiology
*Cardiovascular Diseases/physiopathology/etiology/microbiology
Dysbiosis/complications
Cardiometabolic Risk Factors

@article {pmid41901547,
year = {2026},
author = {Theofilis, P and Iliakis, P and Karanikola, AE and Botis, M and Mavromoustakou, K and Xydis, P and Ktenopoulos, N and Karakasis, P and Leontsinis, I and Chrysohoou, C and Tsioufis, K},
title = {Pleiotropic Effects of Cardiac Resynchronization Therapy on Cardiometabolic Modulation in Heart Failure.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {62},
number = {3},
pages = {},
pmid = {41901547},
issn = {1648-9144},
mesh = {Humans ; *Heart Failure/therapy/physiopathology/metabolism ; *Cardiac Resynchronization Therapy/methods/standards ; Energy Metabolism/physiology ; },
abstract = {Cardiac resynchronization therapy (CRT) is a cornerstone intervention for patients with heart failure (HF) and electrical dyssynchrony, improving quality of life, functional capacity, and survival. Beyond mechanical synchrony, mounting evidence suggests CRT exerts systemic and myocardial cardiometabolic benefits. CRT acutely enhances mechanical efficiency and shifts substrate utilization toward greater oxidation of fatty acids and ketones, effects that correlate with long-term reverse remodeling on cardiac magnetic resonance imaging. Earlier metabolomic profiling demonstrated that CRT normalizes circulating energy metabolites, improving Krebs cycle intermediates and substrate balance between glucose and lipids, while baseline metabolite patterns may differentiate responders from non-responders. These metabolic adaptations accompany favorable changes in diastolic performance, right ventricular function, and ventriculo-arterial coupling. In parallel, improved splanchnic perfusion and reduced congestion may ameliorate gut dysbiosis and endotoxemia, mitigating systemic inflammation. Collectively, these findings position CRT as a therapy capable of both mechanical and metabolic restoration in advanced HF. In this review, we discuss the emerging data on how CRT reconditions myocardial energy metabolism, influences ventricular-arterial interactions, and modulates peripheral and gut-derived metabolic pathways.},
}

Humans
*Heart Failure/therapy/physiopathology/metabolism
*Cardiac Resynchronization Therapy/methods/standards
Energy Metabolism/physiology

@article {pmid41901695,
year = {2026},
author = {Philips, CA and Oommen, TT and Theruvath, AH and Sreemohan, A and Baby, A and Alex, AA and Thomas, S and John, SM and Ahamed, R and Tharakan, A and Augustine, P},
title = {Novel Insights on Clinical Outcomes Using Integrated Shotgun Metagenomic Profiling of the Gut Microbiome, Resistome, and Host Immune-Inflammatory Response in Hospitalized Patients with Decompensated Cirrhosis.},
journal = {Pathogens (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
pmid = {41901695},
issn = {2076-0817},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; *Liver Cirrhosis/microbiology/immunology/mortality ; Male ; *Metagenomics/methods ; Female ; Middle Aged ; Aged ; Hospitalization ; Adult ; India ; Feces/microbiology ; Anti-Bacterial Agents/pharmacology ; },
abstract = {Background and Aims: Sepsis drives mortality in cirrhosis, yet the gut antimicrobial resistance (AMR) landscape remains unmapped in high-burden settings like India. This study aimed to integrate shotgun metagenomics with deep immunophenotyping to define the gut-immune-resistome axis and correlate specific microbial and genetic signatures with clinical outcomes in decompensated cirrhosis. Methods: We analysed 78 hospitalized patients with cirrhosis using stool shotgun metagenomics, multiplex cytokine arrays, and flow cytometry. The microbiome and resistome (AMR genes) were mapped and correlated with disease severity, immune function (monocyte HLA-DR, neutrophil CD64), and clinical endpoints including mortality. Results: Disease severity was characterized by a "Gram-negative bloom" (Klebsiella) alongside pathogenic Enterococcus expansion and novel markers: Clostridium sp. C5-48 (severe decompensation) and Sutterella (ascites). A specific, dense resistome predicted adverse outcomes; the quinolone-resistance gene QnrB4 correlated with mortality and immune paralysis, while the carbapenemase OXA-833 gene was linked to gastrointestinal bleeding. Notably, the commensal Ligilactobacillus salivarius was associated with systemic inflammatory cytokines. Conclusions: This study reveals a "pathogenic ecosystem" in Indian decompensated cirrhosis where the resistome is intrinsically linked to host immune failure. The identification of specific prognostic markers (QnrB4, OXA-833) and inflammatory associations with L. salivarius challenges generic probiotic use and underscores the urgent need for precision, resistome-targeted therapies.},
}

Humans
*Gastrointestinal Microbiome/genetics
*Liver Cirrhosis/microbiology/immunology/mortality
Male
*Metagenomics/methods
Female
Middle Aged
Aged
Hospitalization
Adult
India
Feces/microbiology
Anti-Bacterial Agents/pharmacology

@article {pmid41901728,
year = {2026},
author = {Mougiou, D and Gioula, G and Skoura, L and Minti, F and Karampatakis, T and Malandris, D and Pelekoudas, K and Kachrimanidou, M},
title = {Characterization of the Gut Microbiome of Patients with Clostridioides difficile Infection and Healthy Individuals in Greece.},
journal = {Pathogens (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
pmid = {41901728},
issn = {2076-0817},
mesh = {Humans ; *Gastrointestinal Microbiome ; Male ; Female ; *Clostridium Infections/microbiology ; Middle Aged ; Greece ; Aged ; RNA, Ribosomal, 16S/genetics ; Prospective Studies ; *Clostridioides difficile/genetics ; Adult ; Feces/microbiology ; Aged, 80 and over ; DNA, Bacterial/genetics ; *Bacteria/classification/genetics/isolation & purification ; },
abstract = {BACKGROUND/OBJECTIVES: The gut microbiome plays an important role in the colonization of an individual by Clostridioides difficile and in the development of Clostridioides difficile infection (CDI). The main purpose of this study was to compare the gut microbiomes of patients with CDI and healthy individuals.

METHODS: We prospectively included 48 individuals: 32 patients with CDI and 16 healthy individuals. Microbiomes were analyzed by sequencing the hypervariable regions of the 16S rRNA gene using an Ion GeneStudio™ S5 System. Further statistical analysis of microbiome data was performed with the open-source programming language R version 3.5.2.

RESULTS: Among the CDI patients, Firmicutes and Proteobacteria were the most abundant phyla, while Enterobacteriaceae and Enterococcaceae were the most abundant families. Genus-level analysis showed that Enterococcus was the dominant genus in CDI patients; in contrast, in healthy individuals, Faecalibacterium was the most abundant. The MaAsLin2 tool revealed that members of the family Enterococcaceae and the genus Enterococcus were more abundant in patients with CDI than in healthy individuals. Alpha and beta diversity did not reveal differences between the two study groups.

CONCLUSIONS: We observed differences in microbiome patterns between healthy individuals and CDI patients that were consistent with the literature. Further studies are needed.},
}

Humans
*Gastrointestinal Microbiome
Male
Female
*Clostridium Infections/microbiology
Middle Aged
Greece
Aged
RNA, Ribosomal, 16S/genetics
Prospective Studies
*Clostridioides difficile/genetics
Adult
Feces/microbiology
Aged, 80 and over
DNA, Bacterial/genetics
*Bacteria/classification/genetics/isolation & purification

@article {pmid41901740,
year = {2026},
author = {Pazmiño-Gomez, B and Rodas-Pazmiño, K and Pazmiño-Pérez, R and Tapia-Guijarro, T and Balcazar-Quimi, W and Valle-Asan, S and Salazar-Vera, S and Villalva-Vera, M and Ochoa-Fajardo, D and Rodas-Neira, E},
title = {Native Bacillus-Based Probiotic Consortia Suppress Vibrio parahaemolyticus and Restructure Hatchery Water Microbiomes in Shrimp Larval Systems.},
journal = {Pathogens (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
pmid = {41901740},
issn = {2076-0817},
mesh = {*Probiotics/pharmacology/administration & dosage ; Animals ; *Vibrio parahaemolyticus/drug effects ; *Bacillus/physiology ; *Penaeidae/microbiology/growth & development ; *Microbiota ; Larva/microbiology ; Aquaculture/methods ; Water Microbiology ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Shrimp aquaculture is constrained by opportunistic bacterial pathogens, particularly Vibrio parahaemolyticus, whose proliferation in hatchery systems is shaped by microbial community structure. We evaluated the antagonistic activity and microbiome effects of two native Bacillus-based probiotic consortia (CN5, RS3) applied alone or combined (MIX) in shrimp larval culture water over 30 days, relative to a no-probiotic control. Treatments were assessed using standardized in vitro inhibition assays, 16S rRNA gene (V3-V4) amplicon sequencing, functional inference, and integrative multivariate and structural modeling. All probiotic treatments showed consistently high antagonistic activity against V. parahaemolyticus, whereas the control showed no inhibition. Amplicon profiling indicated treatment-associated microbiome restructuring, with increased Bacillus dominance and reduced relative abundance of Vibrio spp. under probiotic conditions. Multivariate analyses separated probiotic and control groups, and PLS-SEM identified Bacillus dominance as a central driver of antagonistic activity mediated by inferred bioactive functional potential, while water-quality variables had limited direct effects. Probiotics were administered directly to the culture water once daily after routine water exchange to 1 × 10[6] CFU mL[-1] (CN5 or RS3); MIX was applied 1:1 (v/v) at the same total dose.},
}

*Probiotics/pharmacology/administration & dosage
Animals
*Vibrio parahaemolyticus/drug effects
*Bacillus/physiology
*Penaeidae/microbiology/growth & development
*Microbiota
Larva/microbiology
Aquaculture/methods
Water Microbiology
RNA, Ribosomal, 16S/genetics

@article {pmid41901742,
year = {2026},
author = {Kavvada, A and Gioula, G and Protopapas, A and Protopapas, AA and Christoforidi, M and Minti, F and Savopoulos, C and Chatzidimitriou, M},
title = {Characterization of the Gastric Antrum Microbiome in Helicobacter pylori-Negative Individuals: Insights from a Greek Population Using 16S rRNA Next-Generation Sequencing.},
journal = {Pathogens (Basel, Switzerland)},
volume = {15},
number = {3},
pages = {},
pmid = {41901742},
issn = {2076-0817},
mesh = {Humans ; *RNA, Ribosomal, 16S/genetics ; Greece ; Female ; Male ; Middle Aged ; High-Throughput Nucleotide Sequencing ; Adult ; Helicobacter pylori ; *Pyloric Antrum/microbiology ; *Gastrointestinal Microbiome/genetics ; Aged ; *Bacteria/classification/genetics/isolation & purification ; *Microbiota ; Helicobacter Infections/microbiology ; DNA, Bacterial/genetics ; },
abstract = {BACKGROUND: Once considered a sterile organ, the human stomach is now known to harbor a diverse microbial community that may influence both gastric homeostasis and disease. While extensive research has been conducted worldwide, regional variation in the gastric microbiome remains insufficiently characterized. This study aimed to describe the gastric antrum microbiome of Helicobacter pylori-negative Greek adults using 16S rRNA next-generation sequencing (NGS).

METHODS: Samples of gastric biopsies were obtained from patients undergoing gastroscopy at a tertiary hospital in Greece. H. pylori infection was excluded through a combination of bacterial culture and patient medical history. The final study group consisted of 9 subjects. Following DNA extraction, the 16S rRNA gene was sequenced on the Ion Torrent™ platform. Bioinformatic processing and statistical analyses were performed using the phyloseq, vegan, and ggplot2 R packages. Microbial composition, relative abundance, and alpha diversity (Shannon and Inverse Simpson indices) were evaluated at the genus level.

RESULTS: The gastric microbiome comprised 19 phyla, 150 families, 213 genera, and 391 species. The predominant phyla were Proteobacteria (36.92%), Firmicutes (34.21%), and Bacteroidetes (12.97%). The most prevalent families were Streptococcaceae, Helicobacteraceae, Prevotellaceae, and Pasteurellaceae. At the genus level, Streptococcus (21.71%), Helicobacter (18.39%), and Prevotella (9.99%) accounted for nearly half of the total relative abundance. Alpha diversity indices indicated moderate richness and evenness across samples.

CONCLUSIONS: The gastric antrum microbiome of H. pylori-negative Greek individuals exhibits substantial taxonomic diversity dominated by Proteobacteria and Firmicutes. The microbial community structure aligns closely with profiles reported in other global populations. These findings provide a reference baseline for future comparative analyses involving H. pylori-positive individuals to better understand microbiome shifts associated with colonization and gastric disease.},
}

Humans
*RNA, Ribosomal, 16S/genetics
Greece
Female
Male
Middle Aged
High-Throughput Nucleotide Sequencing
Adult
Helicobacter pylori
*Pyloric Antrum/microbiology
*Gastrointestinal Microbiome/genetics
Aged
*Bacteria/classification/genetics/isolation & purification
*Microbiota
Helicobacter Infections/microbiology
DNA, Bacterial/genetics

@article {pmid41902183,
year = {2026},
author = {Cardoso, MA and Vieira, CSD and Moreira, ICF and Saraiva, FMS and Brito, IAA and Gandara, ACP and Menna-Barreto, RFS and Oliveira, PL and Paes, MC and Pane, A},
title = {Rhodnius prolixus Viruses Interfere with Proliferation and Metacyclogenesis of the Chagas Disease Agent Trypanosoma cruzi.},
journal = {Viruses},
volume = {18},
number = {3},
pages = {},
pmid = {41902183},
issn = {1999-4915},
support = {428100/2018-0//National Council for Scientific and Technological Development (CNPq)/ ; E-26/210.339/2024//the Research Support Foundation of the State of Rio de Janeiro/ ; },
mesh = {*Trypanosoma cruzi/virology/growth & development ; Animals ; *Rhodnius/virology/parasitology ; *Chagas Disease/parasitology/transmission ; Insect Vectors/virology/parasitology ; },
abstract = {The protozoan Trypanosoma cruzi is the etiological agent of Chagas disease, a neglected tropical disease that mostly affects the population of Latin American countries, with an estimated 7 million infected people and more than 10,000 deaths per year worldwide. T. cruzi is typically transmitted by hematophagous triatomine insects, with Rhodnius prolixus being a major insect vector in South America. While the microbiome of triatomine insects has been investigated to a certain extent, the ternary interaction between triatomes insects, T. cruzi, and viruses remains virtually unexplored. In this study, we show by transmission electron microscopy and by RT-PCR that Rhodnius prolixus viruses (RpVs) can infect the intestine of R. prolixus, which places them in close contact with the gut microbiota. These observations suggest that T. cruzi can be infected by the insect viruses while transiting through the gut. Here, we show that the RpVs are capable of infecting the epimastigote forms of T. cruzi in vitro and maintain the viral load stabilized for 3 to 7 days after infection. We also show that, at least in the case of the iFlavirus RpV1, viral genomes are detectable in the T. cruzi cytoplasm. Interestingly, R. prolixus ovarian extracts enriched with RpVs decrease epimastigote proliferation and their capacity for differentiation into the ineffective metacyclic trypomastigotes in vitro. Our results start to shed light on the interaction between RpVs and T. cruzi, suggesting possible routes of infection and unveiling a role for viral infections in the development of this important pathogen.},
}

*Trypanosoma cruzi/virology/growth & development
Animals
*Rhodnius/virology/parasitology
*Chagas Disease/parasitology/transmission
Insect Vectors/virology/parasitology

@article {pmid41902219,
year = {2026},
author = {Wang, X and Zhang, J and Chen, J and Huang, Q and Duan, X and Zhu, W},
title = {The Role of Viral Infection and Microbial Dysbiosis in Glaucoma: From Pathogenesis to Therapeutic Strategies.},
journal = {Viruses},
volume = {18},
number = {3},
pages = {},
pmid = {41902219},
issn = {1999-4915},
support = {Grant No. 82471079//the National Natural Science Foundation of China/ ; Grant No. 82501363//the Young Scientists Fund of the National Natural Science Foundation of China/ ; Grant No. 22507154//the Young Scientists Fund of the National Natural Science Foundation of China/ ; Grant No. kq2502222//the Changsha Municipal Natural Science Foundation of China/ ; Grant No. 2025M772429//the Science Foundation for Post Doctorate Research of the Ministry of Science and Technology of China/ ; Grant No. AMF2406D01//the Science and Technology Foundation of Aier Eye Hospital Group of China/ ; },
mesh = {*Dysbiosis/microbiology/complications/therapy ; Humans ; *Glaucoma/microbiology/therapy/virology/etiology ; Animals ; *Virus Diseases/complications ; Gastrointestinal Microbiome ; },
abstract = {Glaucoma is a leading cause of irreversible blindness, yet vision loss often progresses despite effective intraocular pressure (IOP) control, suggesting the involvement of non-hydrodynamic mechanisms. This review explores the potential synergistic interaction between viral persistence and microbial dysbiosis in pathogenesis. While acknowledging that current evidence regarding the microbiome is largely associative and derived from small cohorts or animal models, we analyze how these environmental insults may disrupt autophagic flux and induce immune dysregulation to drive chronic neuroinflammation. Furthermore, we explore theoretical therapeutic strategies targeting this distinct pathological nexus, ranging from metabolic restoration of the gut-eye axis to the repurposing of advanced nanocarriers to overcome ocular barriers. This framework lays the groundwork for next-generation, etiology-based precision management.},
}

*Dysbiosis/microbiology/complications/therapy
Humans
*Glaucoma/microbiology/therapy/virology/etiology
Animals
*Virus Diseases/complications
Gastrointestinal Microbiome

@article {pmid41902239,
year = {2026},
author = {Whitt, TN and Heath, A and Hill, DJ and Brubaker, DK and Farr Zuend, C},
title = {Risk of HSV-2 Acquisition Among Women with Bacterial Vaginosis: Systematic Review and Meta-Analysis.},
journal = {Viruses},
volume = {18},
number = {3},
pages = {},
pmid = {41902239},
issn = {1999-4915},
support = {Start up funds//Case Western Reserve University/ ; },
mesh = {Humans ; Female ; *Vaginosis, Bacterial/complications/virology/microbiology ; *Herpesvirus 2, Human/physiology ; *Herpes Genitalis/virology/epidemiology ; Vagina/microbiology/virology ; Virus Shedding ; Risk Factors ; Microbiota ; },
abstract = {OBJECTIVE: Bacterial vaginosis is a dysbiosis of the vaginal microbiome, typically characterized by a loss of Lactobacillus. Lactobacillus plays a crucial role in vaginal immunity and protection against sexually transmitted infections. Herpes simplex virus 2, the primary cause of genital herpes, impacts 13% of people worldwide. We undertook this systematic review and meta-analysis to examine the risk of herpes simplex virus 2 acquisition in women with bacterial vaginosis. Secondarily, we examined the impact of bacterial vaginosis on herpes simplex virus 2 shedding, reactivation, and symptoms.

DATA SOURCES: We searched PubMed, EMBASE, Cochrane, Web of Science, Google Scholar, and ClinicalTrials.gov for articles published before 1 July 2023 for microbiome and herpes simplex virus type 2. Studies were limited to human subjects and the English language. An updated search was performed in January 2026. This study was registered on PROSPERO (CRD42023439139).

METHODS OF STUDY SELECTION: Studies on non-pregnant, reproductive-aged cisgender women that diagnosed bacterial vaginosis by Amsel Criteria, Nugent Scoring or used molecular techniques, and those that detected herpes simplex virus 2 by serological assay or PCR testing were included. Our search identified 863 results with four publications eligible for inclusion. For our secondary outcomes, 40 results were identified regarding herpes simplex virus 2 shedding, with two publications eligible for inclusion, which did not meet our threshold for meta-analysis. There were 21 results identified for herpes simplex virus 2 reaction and 115 results for herpes simplex virus 2 symptoms, with no articles being eligible for inclusion.

Quality assessment was performed following data extraction using the quality assessment scales from the Joanna Briggs Institute. Results were extracted, and the pooled hazard ratio was calculated with 95% confidence interval. A total of 1906 women were included in this analysis, and 255 acquired herpes simplex virus 2. The pooled unadjusted hazard ratios produced an effect size of 1.91, (95% confidence interval 1.4649-2.4980), and a p-value of <0.0001, while the pooled adjusted hazard ratios produces an effect size of 1.85, (95% confidence interval of 1.3556-2.5162), and a p-value of 0.0001 indicating that bacterial vaginosis is associated with a increased risk of herpes simplex virus 2 acquisition.

CONCLUSIONS: This systematic review with meta-analysis indicates that bacterial vaginosis is associated with a significantly increased risk (91% unadjusted, 85% adjusted) of herpes simplex virus 2 acquisition, indicating that bacterial vaginosis treatment may reduce herpes simplex virus 2 acquisition. A notable limitation of these findings is the relatively small number of studies eligible for inclusion in this systematic review and meta-analysis.},
}

Humans
Female
*Vaginosis, Bacterial/complications/virology/microbiology
*Herpesvirus 2, Human/physiology
*Herpes Genitalis/virology/epidemiology
Vagina/microbiology/virology
Virus Shedding
Risk Factors
Microbiota

@article {pmid41902263,
year = {2026},
author = {Shao, H and Deng, Y and Shi, Y and Duan, Y},
title = {Engineered Bacteriophages: A Next-Generation Platform for Precision Antimicrobials and Therapeutics.},
journal = {Viruses},
volume = {18},
number = {3},
pages = {},
pmid = {41902263},
issn = {1999-4915},
support = {2025YFC3408500//the National Key Research and Development Program of China/ ; 32571872//the National Natural Science Foundation of China/ ; QYPY20230033//the Research Funds of Center for Advanced Interdisciplinary Science and Biomedicine of IHM/ ; WK9100000063//the Fundamental Research Funds for the Central Universities/ ; XDB0940000//the Research Funds of Strategic Priority Research Program of the Chinese Academy of Sciences/ ; GZC20232554//the Postdoctoral Fellowship Program of CPSF/ ; 2024M753097//the China Postdoctoral Science Foundation/ ; WK9100000083//the Fundamental Research Funds for the Central Universities/ ; },
mesh = {*Bacteriophages/genetics ; Humans ; *Phage Therapy/methods ; Animals ; *Precision Medicine/methods ; Genetic Engineering ; Bacterial Infections/therapy ; *Anti-Infective Agents/therapeutic use ; Anti-Bacterial Agents ; },
abstract = {The escalating crisis of antimicrobial resistance (AMR) and the stagnating antibiotic pipeline have renewed interest in bacteriophage therapy. While natural phages offer specificity and low toxicity, their narrow host range, bacterial resistance, and safety concerns limit clinical use. To overcome these hurdles, phages are being engineered using biotechnology. This review outlines the history of phage therapy and systematically summarizes advances in engineered phage preparation, including genetic modification, chemical conjugation, and physical encapsulation. We highlight the application of engineered phages against multidrug-resistant infections, gastrointestinal diseases through gut microbiome modulation, and as targeted delivery vehicles or immune adjuvants in cancer therapy. While significant advances have been made, several critical challenges remain, particularly in regulatory approval, large-scale manufacturing, and ensuring long-term safety. We conclude that engineered phages, as customizable and precise biological tools, are poised to advance precision phage medicine, offering a transformative solution to AMR and fostering convergence across synthetic biology, medicine, and environmental science.},
}

*Bacteriophages/genetics
Humans
*Phage Therapy/methods
Animals
*Precision Medicine/methods
Genetic Engineering
Bacterial Infections/therapy
*Anti-Infective Agents/therapeutic use
Anti-Bacterial Agents

@article {pmid41902328,
year = {2026},
author = {Ganamurali, N and Devarajan, M and Sabarathinam, S},
title = {Microbiome Guided Precision Pharmacology in Pregnancy: Organ Crosstalk, Maternal-Fetal Drug Disposition, and PBPK-Informed Dosing.},
journal = {Comprehensive Physiology},
volume = {16},
number = {2},
pages = {e70138},
doi = {10.1002/cph4.70138},
pmid = {41902328},
issn = {2040-4603},
mesh = {Humans ; Pregnancy ; Female ; *Maternal-Fetal Exchange/physiology ; *Precision Medicine/methods ; *Gastrointestinal Microbiome/physiology ; Pharmaceutical Preparations/metabolism/administration & dosage ; Animals ; Pharmacokinetics ; },
abstract = {Drug therapy during pregnancy poses unique challenges, requiring a balance between maternal benefit and fetal safety. Profound physiological changes, including altered plasma volume, protein binding, hepatic metabolism, renal clearance, and placental transfer, transform pregnancy pharmacology into a dynamic process. Classical concepts such as initiation, loading, maintenance, tapering, and therapeutic monitoring remain fundamental but demand gestation-specific adaptations. This overview integrates fundamental pharmacological concepts with clinical practices tailored for pregnancy, such as personalized dosing, therapeutic monitoring, and structured tapering. Recent studies further underscore the role of the maternal gut microbiome in shaping drug metabolism, absorption, and overall exposure. Variations in how individuals respond to medication during pregnancy may stem from microbial enzymes and metabolites that interact with the body's pharmacokinetic processes. By merging microbiome data with physiologically based pharmacokinetic modeling and pharmacometric tools, clinicians can enhance drug disposition forecasts and refine precision dosing strategies in obstetric care.},
}

Humans
Pregnancy
Female
*Maternal-Fetal Exchange/physiology
*Precision Medicine/methods
*Gastrointestinal Microbiome/physiology
Pharmaceutical Preparations/metabolism/administration & dosage
Animals
Pharmacokinetics

@article {pmid41902480,
year = {2026},
author = {Chugh, RM and Bhanja, P and Schueddig, E and Setianegara, J and Lin, Y and Guida, K and Rehman, S and Krepel, S and Koestler, D and Chen, RC and Cook, KL and Saha, S},
title = {Proton FLASH Exposure Preserves Gut Commensal Microbiomes and Spares Intestinal Stem Cells.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e19249},
doi = {10.1002/advs.202519249},
pmid = {41902480},
issn = {2198-3844},
support = {//This work was supported by a sponsored Research Agreement from IBA to perform preclinical research on FLASH Proton Radiotherapy (KUMC-IBA collaborative fund) and KUCC CCSG (P30 CA168524)./ ; },
abstract = {Emerging evidence shows that Proton FLASH radiotherapy can spare normal tissues while maintaining anti-tumor efficacy. However, its impact on intestinal stem cells (ISCs) and the gut microbiome remains unclear. Gut microbiome influences ISC's radiosensitivity. In a mouse model of abdominal irradiation, Proton FLASH exposure exhibited improved survival and less crypt-villus damage compared to Proton Conventional dose rate. Using scRNA-sequencing, we demonstrated that Proton FLASH exposure using pulsed pencil beam scanning spares two distinct ISC populations, Lgr5+ Crypt-based columnar cells (CBCs) and a Ly6a+, Clu+, Areg+, Anxa2+ revival stem cell (revSC) population-by modulating oxidative stress and cell cycle progression. Analysis of α and β-diversity demonstrated that Proton FLASH modulates gut microbiota composition without compromising overall species richness. Notably, Proton FLASH-irradiated mice had higher abundances of Alistipes sp. and Akkermensia sp., both known for protective effects on ISCs and the intestinal mucosa. The role of microbiome in Proton FLASH-mediated sparing effect was further confirmed by fecal microbiota transplantation, where Proton FLASH-donor microbiota demonstrated reduced lethality with protection of crypt villus morphology in recipient mice exposed to Proton Conventional dose rate. Our findings highlight the crucial role of the microbiome in the Proton FLASH-mediated sparing of the mucosal epithelium.},
}

@article {pmid41902532,
year = {2026},
author = {Belančić, A and Fajkić, A and Sener, YZ and Jelaković, A and Alić, L and Gkrinia, EMM and Verbanac, D and Jelaković, B},
title = {Gut Dysbiosis as a Shared Mechanism in Obesity and Hypertension: Exploring a Promising Therapeutic Avenue.},
journal = {Endocrinology, diabetes & metabolism},
volume = {9},
number = {3},
pages = {e70159},
doi = {10.1002/edm2.70159},
pmid = {41902532},
issn = {2398-9238},
mesh = {Humans ; *Obesity/microbiology/therapy/complications ; *Dysbiosis/therapy/complications/microbiology ; *Gastrointestinal Microbiome/physiology ; *Hypertension/microbiology/therapy/etiology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Animals ; Prebiotics ; },
abstract = {BACKGROUND: Obesity and hypertension are interrelated global health challenges sharing common pathophysiological mechanisms, including insulin resistance, chronic inflammation and neurohormonal dysregulation. Emerging evidence highlights the gut microbiome as a crucial mediator in this interplay, influencing intestinal barrier integrity, systemic inflammation and metabolic homeostasis.

METHODS: In this narrative review, we critically examine the interplay between obesity-induced hypertension and the gut microbiome, evaluating current evidence, therapeutic implications and future research priorities.

RESULTS: Obesity-associated gut dysbiosis disrupts the intestinal epithelial barrier, increasing translocation of bacterial products like lipopolysaccharides into circulation, promoting systemic inflammation that exacerbates insulin resistance, adipose dysfunction and hypertension. Current treatments targeting obesity, from lifestyle modification to bariatric surgery, show beneficial effects on blood pressure, but microbiome-targeted interventions are an evolving therapeutic frontier. Prebiotics, probiotics, synbiotics and faecal microbiota transplantation have demonstrated potential antihypertensive effects in preclinical and clinical studies, although findings are heterogeneous and require confirmation in larger randomised trials. Methodological challenges remain, including the need for advanced microbial sampling techniques beyond faecal analysis to fully capture disease-relevant microbiota alterations.

CONCLUSION: This review synthesises current knowledge on gut microbiome involvement in obesity-induced hypertension, evaluates microbiome-based therapeutic strategies and identifies critical research gaps to guide future investigations aimed at mitigating the dual pandemics of obesity and hypertension.},
}

Humans
*Obesity/microbiology/therapy/complications
*Dysbiosis/therapy/complications/microbiology
*Gastrointestinal Microbiome/physiology
*Hypertension/microbiology/therapy/etiology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Animals
Prebiotics

@article {pmid41902691,
year = {2026},
author = {Lewis, GS and Adejumo, S and Reczek, S and Malas, J and Ramanauskas, K and Walker, JF and Cook, MD and Horswill, CA and Hampton-Marcell, J},
title = {The athlete microbiome project: Integrating deep learning to reveal microbial associations of physical fitness.},
journal = {Physiological genomics},
volume = {},
number = {},
pages = {},
doi = {10.1152/physiolgenomics.00278.2025},
pmid = {41902691},
issn = {1531-2267},
abstract = {Regular physical training improves human fitness and health through direct effects on muscle and metabolism and indirect effects via alterations in gut microbiome composition. To determine whether athletes harbor a distinct gut microbiome and whether microbiome composition associates with established markers of physical fitness, VO2max and percent fat-free mass, we conducted a secondary analysis of amplicon sequencing data and metadata from published human microbiota studies across three continents. Participants were categorized as athletes (n = 656) or non-athletes (n = 199). Using multivariate statistics, random forest models, and a multilayer perceptron neural network, we identified structured differences in gut microbiome composition, associated with fitness metrics and athletic status. Random forest regression models explained up to 63% of the variance in percent fat-free mass and 45% in VO2 max, with taxa such as Faecalibacterium, Megamonas, Bifidobacterium, and Blautia ranking among the most informative predictive features across analyses. Classification models further demonstrated that athletic status could be predicted from microbiome composition: a mixed-effects-informed random forest achieved a balanced accuracy of 71%, while a multilayer perceptron captured coordinated, multivariate microbial patterns and achieved stable performance across stratified five-fold cross-validation and an independent, held-out test set comprising 20% of samples not used during model training (balanced accuracy = 0.91; AUC = 0.97). Together, these findings indicate that athletic status and fitness-related traits are associated with gut microbiome compositional patterns, highlighting candidate taxa for mechanistic validation and demonstrating the utility of integrative machine learning for distinguishing athletes from non-athletes.},
}

@article {pmid41902956,
year = {2026},
author = {Christoph, HAM and Kimble, SJA},
title = {Hydroelectric Dam May Impact the Microbiome of an Endangered Northern Map Turtle (Graptemys geographica) Population.},
journal = {Current microbiology},
volume = {83},
number = {5},
pages = {},
pmid = {41902956},
issn = {1432-0991},
support = {529//Maryland Department of Natural Resources/ ; 52008712//Towson University/ ; },
abstract = {UNLABELLED: Classified as state-endangered, Maryland’s population of Northern Map Turtles (NMTs) (Graptemys geographica) faces habitat alteration and fragmentation due to the Conowingo Hydroelectric Dam and other factors. Maryland’s NMTs also reside in an urbanized area with high levels of human activity, which leads to overall disturbance and pollution. The combined impacts of these stressors could be affecting the health of NMTs and may contribute to future decline. The microbiome has been explored as an indicator of organismal health in other species and can be used to inform wildlife management strategies. We collected cloacal (n = 35) and oral (n = 34) microbiome swabs from wild NMTs at four different sites along the Maryland portion of the Susquehanna River in 2022. Using 16 S rRNA sequencing, results suggested that the dam plays a significant role in determining cloacal and oral microbiome structure, with bacteria associated with pollution and disease being significantly more prevalent above the dam. Of note are Acinetobacter spp., which is associated with heavy metal contamination, and Aeromonas spp., which is associated with shell disease in map turtles. Despite the known dietary dimorphism of NMTs, we did not find significant differences in the microbiomes of males and females. The impact that dams have on microbiomes and wildlife is not well understood, and these results may help to enact more specific management strategies in these systems. Our findings will contribute to the conservation of an endangered freshwater turtle population while adding to the limited breadth of knowledge of reptilian health.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00284-026-04846-w.},
}

@article {pmid41903008,
year = {2026},
author = {Heyse, J and Props, R and Defoirdt, T and Boon, N},
title = {Life strategies of bacterial taxa in rearing water microbiomes of whiteleg shrimp (Litopenaeus vannamei) larviculture.},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {4},
pages = {},
pmid = {41903008},
issn = {1573-0972},
support = {1S80618N//Fonds Wetenschappelijk Onderzoek/ ; 1221020N//Fonds Wetenschappelijk Onderzoek/ ; },
}

@article {pmid41903026,
year = {2026},
author = {Wolthuis, JC and Schultheiss, JPD and Magnúsdóttir, S and Stigter, E and Tang, YF and Jans, J and Oldenburg, B and de Ridder, J and van Mil, S},
title = {Univariate- and machine learning-based plasma metabolite signature differentiates PSC-IBD from IBD and is predicted to be driven by gut microbial changes.},
journal = {Metabolomics : Official journal of the Metabolomic Society},
volume = {22},
number = {2},
pages = {},
pmid = {41903026},
issn = {1573-3890},
mesh = {Humans ; *Machine Learning ; *Gastrointestinal Microbiome ; *Inflammatory Bowel Diseases/diagnosis/blood/metabolism/microbiology ; *Cholangitis, Sclerosing/diagnosis/blood/metabolism ; *Metabolomics/methods ; Male ; Female ; Biomarkers/blood ; Adult ; Middle Aged ; Crohn Disease/diagnosis/blood ; Colitis, Ulcerative/diagnosis/blood/metabolism ; Metabolome ; Mass Spectrometry ; },
abstract = {INTRODUCTION: Inflammatory bowel disease (IBD) is a group of chronic inflammatory conditions of the gastrointestinal tract comprising two major phenotypes, Crohn's disease (CD) and ulcerative colitis (UC). Up to 8% of patients with IBD also develop primary sclerosing cholangitis (PSC), characterised by cholestasis and progressive destruction of the biliary tree, resulting in cirrhosis, end-stage liver disease and cholangiocarcinoma. Clinical outcome can currently not be improved through medication, denoting the importance of diagnosis prior to irreversible damage, which requires biomarkers of (early) disease.

OBJECTIVES: We employed direct infusion mass spectrometry (DI-MS)-based metabolomics on plasma to build predictive, potentially diagnostic models for PSC-IBC and other phenotypes including IBD subtype, stricture and fistula presence and more. We used this dataset to simultaneously investigate aetiology of these phenotypes.

METHODS: Samples of 348 IBD patients were included for analysis. The data was analysed using our previously reported tool, MetaboShiny. We built predictive models using Random Forest (RF), and subsequently combined with univariate statistics to rank m/z features connected to PSC-IBD. This ranking was used to perform mummichog enrichment analysis connected to metabolic and metagenomic changes.

RESULTS: The highest performing predictive model differentiated PSC-IBD from PSC. The metabolic signature was enriched in changes to amino acid and vitamin metabolism, alongside changes to the metagenome suggesting decreases in anti-inflammatory microbial species and increases in pro-inflammatory species.

CONCLUSION: These results demonstrate the potential of DI-MS-based metabolomics with machine learning to create diagnostic models and generate hypotheses on the metabolomic-metagenomic level. Sharing our dataset of patients will enrich future human IBD metabolomics research possibilities.},
}

Humans
*Machine Learning
*Gastrointestinal Microbiome
*Inflammatory Bowel Diseases/diagnosis/blood/metabolism/microbiology
*Cholangitis, Sclerosing/diagnosis/blood/metabolism
*Metabolomics/methods
Male
Female
Biomarkers/blood
Adult
Middle Aged
Crohn Disease/diagnosis/blood
Colitis, Ulcerative/diagnosis/blood/metabolism
Metabolome
Mass Spectrometry

@article {pmid41903028,
year = {2026},
author = {Reytor-González, C and Verde, L and Annunziata, G and Román-Galeano, NM and Horowitz, R and Galasso, M and Muscogiuri, G and Frias-Toral, E and Simancas-Racines, D and Barrea, L},
title = {The Role of Gut Microbiota in Postmenopausal Women: Implications for Lipid Metabolism and Targeted Nutritional Interventions.},
journal = {Current nutrition reports},
volume = {15},
number = {1},
pages = {},
pmid = {41903028},
issn = {2161-3311},
abstract = {PURPOSE OF REVIEW: This review explores the complex interplay between menopause, estrogen decline, lipid metabolism, and gut microbiota alterations. It highlights the physiological and metabolic changes that predispose postmenopausal women to dyslipidemia and increased cardiovascular disease risk, with particular emphasis on the emerging role of the gut microbiota in modulating lipid homeostasis and inflammatory pathways. In addition, it examines the therapeutic potential of microbiota-targeted nutritional strategies to restore metabolic balance and improve cardiometabolic outcomes in postmenopausal women.

RECENT FINDINGS: Recent clinical and experimental evidence indicates that menopause-related hormonal changes and aging are associated with gut microbiota dysbiosis, which may contribute to adverse lipid profiles through mechanisms involving bile acid metabolism, short-chain fatty acid production, and low-grade systemic inflammation. Associations between specific microbial taxa and lipid metabolic patterns have been reported; however, findings remain heterogeneous and causal relationships are difficult to establish due to confounding factors such as diet, lifestyle, and medication use. Nutritional interventions aimed at modulating the gut microbiota—including Mediterranean, plant-based, and DASH dietary patterns, increased dietary fiber intake, and supplementation with prebiotics, probiotics, polyphenols, phytoestrogens, and omega-3 fatty acids—have shown potential to improve lipid profiles and cardiometabolic risk markers.

SUMMARY: The gut microbiota emerges as a relevant contributor to menopause-associated dyslipidemia and cardiovascular risk. While microbiota-targeted nutritional strategies are promising, further longitudinal and interventional studies are needed to clarify causal pathways and identify clinically actionable microbial signatures. Integrating microbiome-informed nutritional approaches into clinical practice may represent a future strategy to improve cardiometabolic health in postmenopausal women.},
}

@article {pmid41903042,
year = {2026},
author = {Lu, GL and Zhao, YH and Ruan, YQ and Ning, J and Wei, L},
title = {Vitamin C modulates Cr(VI)-induced parallel disruptions along the microbiota-gut-brain axis in adult zebrafish: insights from transcriptomic and microbiome analysis.},
journal = {Fish physiology and biochemistry},
volume = {52},
number = {2},
pages = {},
pmid = {41903042},
issn = {1573-5168},
support = {ZDYF2023SHFZ139//Key Research and Development Program of Hainan/ ; 32060169//National Natural Science Foundation of China/ ; KYQD(ZR)21138//Scientific Research Start-up Fund of Hainan University/ ; },
mesh = {Animals ; *Chromium/toxicity ; *Zebrafish/microbiology ; *Gastrointestinal Microbiome/drug effects ; *Ascorbic Acid/pharmacology ; *Brain/drug effects/metabolism ; *Water Pollutants, Chemical/toxicity ; *Transcriptome/drug effects ; RNA, Ribosomal, 16S ; Gene Expression Profiling ; },
abstract = {Hexavalent chromium (Cr(VI)) is a widely present carcinogenic environmental pollutant, has demonstrated well-documented neurotoxic and enterotoxic effects in aquatic organisms, yet limited research exists on mitigating its toxicity through brain-gut-microbiota axis regulation. Vitamin C (VC), a potent antioxidant and immunomodulator, has shown potential in mitigating heavy metal toxicity. Nevertheless, how VC regulates Cr(VI) toxicity via the brain-gut-microbiota axis remains unclear. To investigate VC's potential protective role, adult zebrafish were divided into three groups: control, 2 mg/L Cr(VI), 2 mg/L Cr(VI) + 2 mg/L VC groups, with a 60-day exposure period. Histopathological changes, 16S rRNA, intestinal, and brain RNA-sequencing were examined. The results showed that VC modulated neuropathological lesions and intestinal goblet cell vacuolization caused by Cr(VI). 16S rRNA further confirmed VC partially modulated microbiota homeostasis. Transcriptomic analysis identified 78 differentially expressed genes (DEGs) in the brain; KEGG enrichment analysis showed these DEGs are associated with neurological function and gastrointestinal carcinogenesis pathways. Concurrently, 52 DEGs in intestinal were linked to viral infection and neural signaling pathways. Correlation analyses demonstrated pathogenic Aeromonas was positively correlated with ace, enpep, prss1, asah2, and cd36 in the brain, those are downregulated DEGs, whereas beneficial Pseudomonas was positively correlated with c6ast4 and nfe211b in intestinal, they are upregulated DEGs. This indicates Aeromonas and Pseudomonas could act as key mediators through which VC reduces Cr(VI)-induced neuro- and immunotoxicity. Collectively, these findings provide mechanistic insights into VC's protective role against parallel disruptions along the microbiota-gut-brain axis, suggesting its potential as a waterborne supplement for reducing Cr(VI) toxicity in aquaculture system.},
}

Animals
*Chromium/toxicity
*Zebrafish/microbiology
*Gastrointestinal Microbiome/drug effects
*Ascorbic Acid/pharmacology
*Brain/drug effects/metabolism
*Water Pollutants, Chemical/toxicity
*Transcriptome/drug effects
RNA, Ribosomal, 16S
Gene Expression Profiling

@article {pmid41903043,
year = {2026},
author = {Guhanraj, R and Prathiviraj, R},
title = {Bacteriocins as precision antimicrobials: genomic exploration and oral applications of Lactobacillus peptides.},
journal = {Archives of microbiology},
volume = {208},
number = {6},
pages = {},
pmid = {41903043},
issn = {1432-072X},
}

@article {pmid41903083,
year = {2026},
author = {Zhang, JR and Li, YW and Chen, HX and Luo, Y and Liu, RM and Wang, JB and Liu, NN and Xiao, JH},
title = {Chronic Excessive Exposure to Fluoride Impairs the Intestinal Mucosal Barrier to Cause Inflammatory Response and Microbiome Dysbiosis in Rats.},
journal = {Biological trace element research},
volume = {},
number = {},
pages = {},
pmid = {41903083},
issn = {1559-0720},
support = {QKHJ-ZK[2021]485//Guizhou Provincial Department of Science and Technology/ ; GKFZ-2018-29//Ministry of Science and Technology of the People's Republic of China/ ; 82260158//National Natural Science Foundation of China/ ; QJJ [2023] 020//Department of Education of Guizhou Province/ ; QKHPT-RC-GCC [2022]001-2; QKHJC-ZK[2025]ZD-031//Guizhou Provincial Department of Science and Technology, China/ ; ZSKH-SYS[2025]-03; ZSKHHZ-[2023]-198//Science and Technology Bureau of Zunyi City/ ; },
}

@article {pmid41903099,
year = {2026},
author = {Sumona, AA and Hossen, MB and Hadi, SB and Haque, MA and Haider, MN and Hossain, MT and Alam, MS},
title = {Host-derived Probiotics Enhance Immune Response and Gut Microbiome in the Freshwater Prawn Macrobrachium rosenbergii.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {41903099},
issn = {1867-1314},
}

@article {pmid41903138,
year = {2026},
author = {Zheng, W and Wu, C and Wang, Y and Yan, X and Han, W and Liu, X and He, C and Chen, X and Zhou, X and Zhang, L and Liu, C and Xu, J and Wang, J and Yuan, X and Song, W and Wang, X and Liang, S and Huang, J and Zhang, Y and Yang, R and Zhang, L and Qin, N and Ma, X and Xu, Q and Li, G},
title = {Mutation elevation and functional alterations in Escherichia coli are pertinent to the onset of gestational diabetes mellitus.},
journal = {Cell reports},
volume = {45},
number = {4},
pages = {117143},
doi = {10.1016/j.celrep.2026.117143},
pmid = {41903138},
issn = {2211-1247},
abstract = {In the gut microbiome, purifying selection clears deleterious mutations. However, it is unknown whether this selection pressure is modifiable or what its health implications are. Here, we studied metagenomic and metabolic changes linked to gestational diabetes mellitus (GDM), and observed an increase in Escherichia coli (E. coli) mutations during host pregnancy, linking these genetic changes to host physiology. Severe depletion of bacterial genes before GDM onset was mostly traced to E. coli despite its stable abundance-indicating that functional genetic signals outweigh taxonomic shifts. E. coli and related microbes displayed pregnancy-linked single nucleotide polymorphism elevation, enriched at GDM onset in loci encoding membrane and biofilm components. These pangenomic alterations correlated with handicapped intermicrobial interactions of E. coli and with host serum metabolic abnormalities. We propose that pregnancy relaxes purifying selection, permitting mutation elevation in certain gut bacteria. Resulting functional deficits, potentially through altered ecology and metabolism, may subsequently impact host glucose regulation.},
}

@article {pmid41903152,
year = {2026},
author = {Li, WK and Liu, B and Xu, SF and Shi, JS and Li, J and Liu, J},
title = {Antiepileptic Effects of Hua-Feng-Dan Against Pentylenetetrazol-Induced Seizures in Mice.},
journal = {BioMed research international},
volume = {2026},
number = {1},
pages = {e5336509},
pmid = {41903152},
issn = {2314-6141},
support = {82560832//National Natural Science Foundation of China/ ; U1812403//National Natural Science Foundation of China/ ; 82460879//National Natural Science Foundation of China/ ; 82360859//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Pentylenetetrazole ; Mice ; *Seizures/drug therapy/chemically induced ; *Anticonvulsants/pharmacology/therapeutic use ; Male ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; Disease Models, Animal ; Brain/drug effects/metabolism ; Kindling, Neurologic/drug effects ; Gastrointestinal Microbiome/drug effects ; },
abstract = {Hua-Feng-Dan is a Chinese medicine in the treatment of epilepsy and neurodegeneration. The prior studies demonstrated its protection against neuroinflammation, dopaminergic neuron loss, and in the treatment of ischemic stroke, but its anticonvulsive efficacy against epilepsy remains elusive. The aim of this study was to examine antiepileptic effects of Hua-Feng-Dan recipes and the mechanism of protection. Pentylenetetrazol (PTZ)-induced kindling mouse model (35 mg/kg, ip on alternate days × 10) was used to evaluate the antiepileptic effects of Hua-Feng-Dan recipes. Mice were given original, reduced, and nonfermented Hua-Feng-Dan via feed at clinical dose (0.5 g/kg) and diazepam was used as a positive control. The seizure scores were recorded after each PTZ injection. At the end of the experiments, the brain and colon content were collected for RNA-Seq and 16S rRNA-Seq, respectively, followed by bioinformatics and qPCR verification. Hua-Feng-Dan recipes were effective against PTZ-induced seizures, with original the best and half of reduced (0.25 g/kg) ineffective. PTZ-induced aberrant gene expressions in the brain were ameliorated by Hua-Feng-Dan recipes to various extents. Ingenuity Pathway Analysis of differentially expressed genes revealed that PTZ-altered canonical pathways and upstream regulators were attenuated by Hua-Feng-Dan treatments. qPCR verified the expression of early immediate genes, proinflammatory mediators, transporters and apoptosis genes. PTZ-disrupted gut microbiome was also ameliorated by Hua-Feng-Dan recipes, and the modulation of Lachnospiraceae and ASV230 was consistent with the literature. Hua-Feng-Dan recipes were effective against PTZ-induced kindling mice. The mechanisms appeared to be related to the modulation of brain gene expression and gut microbiota. • Hua-Feng-Dan (HFD) recipes were effective against PTZ-induced seizures in mice. • HFD ameliorated abnormal brain gene expressions in PTZ kindling mice via RNA sequencing (RNA-seq). • IPA of DEGs revealed improved canonical pathways and upstream regulators. • 16S rRNA-seq showed microbiome modulation by HFD in PTZ kindling mice. • qPCR verified selected brain genes and bacterial ASVs.},
}

Animals
*Pentylenetetrazole
Mice
*Seizures/drug therapy/chemically induced
*Anticonvulsants/pharmacology/therapeutic use
Male
*Drugs, Chinese Herbal/pharmacology/therapeutic use
Disease Models, Animal
Brain/drug effects/metabolism
Kindling, Neurologic/drug effects
Gastrointestinal Microbiome/drug effects

@article {pmid41903180,
year = {2026},
author = {Xu, Y and Akinbi, H and Shen, Z and Zhu, J and Shi, L and Du, L and Haslam, DB},
title = {Clinical Care Practices Shape Microbiome-Associated Bloodstream Infection Risk in Geographically Distinct NICUs.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {},
number = {},
pages = {},
doi = {10.1093/cid/ciag213},
pmid = {41903180},
issn = {1537-6591},
abstract = {BACKGROUND: Bloodstream infections (BSI) remain a major cause of morbidity and mortality in preterm infants. Although BSI pathogens vary geographically, the role of local microbial colonization patterns and clinical practices in driving these differences is not well understood.

METHODS: We conducted a prospective cohort study on 127 preterm infants from two geographically distinct NICUs: University of Cincinnati Medical Center (UCMC, USA) and Children's Hospital, Zhejiang University School of Medicine (ZCH, China). Six hundred and sixty-nine longitudinal stool and skin samples collected during the first three weeks of life underwent metagenomic sequencing. Associations between microbiome composition, clinical factors, and BSI epidemiology were evaluated using Generalized Linear Mixed Models and Random Forest.

RESULTS: Distinct gut and skin microbiome profiles were observed between NICUs and corresponded closely with local BSI patterns. Staphylococcus aureus predominated at UCMC, while Klebsiella pneumoniae and Enterococcus species were more common at ZCH. Skin microbiota showed strong association with BSI isolates, implicating the skin as an underrecognized potential reservoir for pathogen translocation. Linear mixed models and Random Forest machine learning approaches revealed that clinical practices, including intravenous catheter placement and antibiotic exposure had greater influence on microbiome composition than geographic location alone.

CONCLUSIONS: Our findings demonstrate that modifiable clinical care practices shape the developing microbiome of preterm infants and contribute to geographic differences in BSI epidemiology. The skin microbiome represents a potentially significant risk factor for invasive infection. Further work to clarify how specific clinical practices influence pathogen colonization may inform strategies to reduce BSI incidence in preterm infants.},
}

@article {pmid41903388,
year = {2026},
author = {Howell, S and Cumpa, G and Masel, BE},
title = {Altered gut microbiome and post traumatic hypopituitarism in chronic TBI: The need for recognition, evaluation and treatment.},
journal = {Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society},
volume = {84},
number = {},
pages = {101688},
doi = {10.1016/j.ghir.2026.101688},
pmid = {41903388},
issn = {1532-2238},
abstract = {Post traumatic hypopituitarism (PTHP) occurs in 30-50% of individuals with chronic moderate-severe TBI as well as individuals with mild TBIs who remain symptomatic after a year. Growth hormone deficiency (GHD) occurs in approximately 15-20%, Gonadotropin deficiencies in 10%, as well as Thyroid and Adrenocorticotropin deficiencies in 4-12%. Individuals frequently have more than one deficiency. These numbers cover a wide range and vary based on time of testing, cut-points and methods used. Recent studies have shown hypoaminoacidemia and altered gut microbiome in a subset of individuals with mTBIs with subjective complaints of fatigue and altered cognition: Brain Injury Associated Fatigue and Altered Cognition (BIAFAC). These individuals may become symptomatic months to years after the injury and frequently have a diminished response to growth hormone stimulation testing, although not always below the established cut points for Growth Hormone Deficiency (GHD). Recognition of BIAFAC for its similarities and differences from PTHP by physicians dealing with TBI will lead to more thorough evaluations and may eventually lead to better treatment options for these individuals. This paper will begin with a discussion of the relevance of anatomy to post -TBI changes, and how hypoaminoacidemia may play a role in the symptoms after TBI.},
}

@article {pmid41903508,
year = {2026},
author = {Pachinger, L and Stukenbrock, EH},
title = {Antimicrobial effectors of plant-associated fungi: multipurpose proteins with fast-evolving surfaces and structurally conserved cores.},
journal = {Current opinion in microbiology},
volume = {91},
number = {},
pages = {102744},
doi = {10.1016/j.mib.2026.102744},
pmid = {41903508},
issn = {1879-0364},
abstract = {Plants are exposed to a variety of devastating pathogens, causing significant yearly yield losses. In order to facilitate infections, plant pathogens secrete an arsenal of molecules termed effectors, which are known to modulate plant immune responses. Plants, on the other hand, possess receptors allowing them to detect invading pathogens by either recognising conserved molecules associated with invading microbes or by perceiving effector molecules. For decades, molecular phytopathology research has been focused on the bilateral molecular crosstalk between plants and pathogens and has deepened our understanding of virulence and defence mechanisms. In recent years, the impact of the plant microbiome on plant-pathogen interactions has gained interest, given the fact that some microbes can aid protection against invading pathogens, and pathogen invasion substantially modulates microbiome composition. Several antimicrobial effectors have been identified in fungal plant pathogens, pointing to direct mechanisms whereby pathogens can alter their hosts' microbiome to promote host colonisation. These new findings highlight that some effectors may have several functions targeting plant processes and fungi or bacteria associated with the plant. Advances in computational biology have greatly enhanced the analysis of predicted effector proteins and revealed that these often are highly conserved among phylogenetically distant fungi. Comparative analyses of protein structures have also revealed that functional divergence may emerge from changes in surface frustration around conserved protein folds. Further, computational simulations of protein evolution indicate that protein properties associated with (antimicrobial) effectors can emerge rapidly around conserved folds. We here summarise and discuss recent studies based on computational biology methods, providing novel insights into effector origin, evolution, and functional divergence.},
}

@article {pmid41903526,
year = {2026},
author = {Bloom, SM and Symul, L and Elsherbini, J and Xu, J and Hussain, S and Shih, J and Sango, A and Mitchell, CM and Hemmerling, A and Parks, TP and Kannan, A and Hussain, FA and Cohen, CR and Holmes, SP and Kwon, DS},
title = {Vaginal microbiota impacts of a Lactobacillus crispatus live biotherapeutic and predictors of colonization in randomized controlled trial.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.003},
pmid = {41903526},
issn = {1934-6069},
abstract = {Bacterial vaginosis (BV) affects >25% of women worldwide and often recurs after standard-of-care metronidazole (MTZ) treatment. LACTIN-V, a live biotherapeutic product (LBP) containing Lactobacillus crispatus strain CTV-05, significantly reduced recurrent BV in a phase 2b clinical trial, but efficacy was incomplete. Here, we characterize microbiota and immune effects using multi-omics and define correlates of treatment success. By week 12, an L. crispatus-dominant microbiota was achieved in 30% of LBP recipients compared with 9% of placebo recipients (benefit ratio: 3.31; p < 0.005). This is primarily due to CTV-05, but native L. crispatus strains are also present and increase over time. Inflammatory cytokines decrease in both arms after MTZ but return to baseline in placebo recipients. Successful L. crispatus colonization is associated with pre-MTZ microbiota, baseline inflammatory profiles, post-MTZ bacterial load, and clinical and behavioral variables. These findings elucidate LBP microbiota effects and identify predictors of treatment success, informing improved intervention strategies to advance women's health.},
}

@article {pmid41903527,
year = {2026},
author = {Salazar, V and Espenschied, ST and Fernandez, AP and Karell, PE and Sangwan, N and Stappenbeck, TS},
title = {The skin microbiota drives cutaneous immune checkpoint inhibitor toxicity in genetically susceptible mice.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.008},
pmid = {41903527},
issn = {1934-6069},
abstract = {Immune checkpoint inhibitors (ICIs) show increasing promise for cancer therapy. However, patients can experience adverse events, particularly those with pre-existing autoimmune disease. We determined that the microbiome can drive ICI-induced systemic toxicity in a mouse model of autoimmune susceptibility. Specifically, ICI treatment of specific pathogen-free (SPF) Act1[-/-] mice, which develop spontaneous autoimmunity due to a deficiency in an immune adaptor, resulted in systemic adverse events that were ameliorated by topical antibiotics. Moreover, germ-free (GF) Act1[-/-] mice failed to develop ICI toxicity. Transfer of gut or skin microbiota from SPF Act1[-/-] mice to GF Act1[-/-] mice showed that only the skin microbiota rendered exGF mice sensitive to ICI toxicity. Notably, therapeutic application of topical antibiotics decoupled ICI-induced toxicity from anti-tumor efficacy in SPF Act1[-/-] mice. This model provides a paradigm for future translational studies in cancer patients to mitigate adverse effects of ICIs and maximize their efficacy by targeting skin microbes.},
}

@article {pmid41903570,
year = {2026},
author = {Wang, X and Jia, Y and Wang, C and Li, D and Guo, X and Jiang, S and Zhou, Z and Gao, C and Wang, F},
title = {Decoding serotonin in endometriosis: unveiling its role in disease pathogenesis via the gut-reproductive microbiota axis.},
journal = {Human reproduction (Oxford, England)},
volume = {},
number = {},
pages = {},
doi = {10.1093/humrep/deag047},
pmid = {41903570},
issn = {1460-2350},
support = {20200601011JC//Jilin Provincial Key Laboratory of Precision Infectious Diseases/ ; 3D5200117426//Key Laboratory of Health and Family Planning Commission of Jilin Province/ ; },
abstract = {STUDY QUESTION: How can the potential mechanisms and targets of endometriosis be explored through multi-omics and multi-location approaches?

SUMMARY ANSWER: This exploration of the gut-reproductive axis in patients with endometriosis found that serotonin is elevated in endometriosis and promotes disease progression through enhanced cell proliferation and inflammation.

WHAT IS KNOWN ALREADY: Endometriosis is a common inflammatory disease. Recent studies indicate that peripheral serotonin, which is regulated by the gut microbiota, can promote the progression of irritable bowel syndrome and various cancers.

STUDY DESIGN, SIZE, DURATION: This cross-sectional study enrolled 22 endometriosis patients and 22 control patients with uterine fibroids (surgical cases, October 2022-June 2023). Samples of vaginal secretions, endometrial tissue, peritoneal lavage fluid, feces, and ectopic lesions were collected from both groups. For validation, serum samples were added from 20 additional endometriosis patients and 20 healthy reproductive-age volunteers.

This study employed 16S rRNA gene sequencing to analyze the microbiota in the vagina, endometrial tissue, peritoneal fluid, and feces of patients with endometriosis and control groups, complemented by untargeted metabolomic analysis of peritoneal fluid. The results identified serotonin as a key metabolite and revealed specific bacterial species, shared between the reproductive and gastrointestinal tracts of endometriosis patients, which were significantly correlated with serotonin levels. Mendelian randomization analysis was conducted to explore the relationship between serotonin, these bacterial species, and endometriosis. Serum serotonin levels in endometriosis patients, BALB/C mouse models, and their respective controls were measured using ELISA. Immunohistochemistry and fluorescence staining were used to detect the expression of serotonin and its receptors in both ectopic and normal endometrium. The effects of serotonin on the biological behavior of various endometriosis cell models, including proliferation, migration, invasion, and apoptosis, were investigated using CCK8 assay, wound healing test, Transwell assay, apoptosis detection, ELISA, transcriptomics, and qPCR. The impact of serotonin on BALB/C mouse models was evaluated using H&E staining, flow cytometry, and ELISA.

We identified a significant enrichment of Akkermansia muciniphila (a bacterium shared by the gut and reproductive tract) in endometriosis patients, which positively correlated with peritoneal serotonin levels; Mendelian randomization analysis linked both to elevated endometriosis risk. Serotonin levels were elevated in patients' serum (using mouse models) and in ectopic endometrium, in comparison to those of controls. In vitro, serotonin boosted endometriosis cell proliferation, migration, invasion, and inflammation, with upregulated IL-17/NF-κB pathways. In mice, serotonin treatment increased lesion growth, cell proliferation, and inflammation.

LARGE SCALE DATA: N/A.

(a) The relatively limited sample size, together with potential imbalance in endometriosis ASRM stage distribution and cesarean section rates, may restrict the generalizability of our findings. In addition, due to the requirement for peritoneal lavage fluid collection, the control group could not consist of entirely healthy women, which may have resulted in a more conservative estimation of group differences. Serum sex hormone levels were not assessed; however, strict inclusion criteria and uniform surgical timing were applied to minimize hormonal confounding. Future studies incorporating cycle-phase-standardized hormone measurements may provide additional insights. (b) Dietary information was not collected in this study, despite the known influence of diet on gut microbiota composition and serotonin metabolism. (c) The direct causal relationship between Akkermansia muciniphila and elevated serotonin levels remains to be established and warrants further validation using germ-free mouse models or fecal microbiota transplantation approaches. (d) The precise mechanisms by which the gut-reproductive tract microbiota axis regulates local and systemic serotonin synthesis remain unclear and require further investigation.

Our study is the first to utilize a multi-omics approach combined with a joint analysis of the female gut-reproductive tract axis across multiple loci, revealing and validating a significant increase in serotonin levels in patients with endometriosis. This change may be regulated by the gut-reproductive microbiota axis. These findings provide new insights into the pathogenesis of endometriosis and identify potential targets for prevention and treatment.

This study was funded by the Jilin Provincial Key Laboratory of Precision Infectious Diseases (Grant No. 20200601011JC), Key Laboratory of Health and Family Planning Commission of Jilin Province (Grant No. 3D5200117426). The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

TRIAL REGISTRATION NUMBER: ChiCTR2300077490.},
}

@article {pmid41903668,
year = {2026},
author = {Brahmachary, P and Keim, EA and Walk, ST and McGee-Lawrence, ME and June, RK},
title = {AhR signaling in joint homeostasis and disease.},
journal = {Biochimie},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.biochi.2026.03.003},
pmid = {41903668},
issn = {1638-6183},
abstract = {The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that integrates environmental, microbial, and metabolic signals to regulate gene expression across diverse tissues. Recent studies highlight AhR's role in skeletal homeostasis and joint biology, particularly through its interactions with microbiome-derived tryptophan metabolites and the Wnt/β-catenin signaling pathway. This review synthesizes current knowledge on AhR signaling mechanisms, including canonical and non-canonical pathways, and explores the impact of exogenous toxicants and microbiome-derived compounds and endogenous host metabolites that activate AhR. We discuss emerging evidence linking AhR activity to cartilage development, inflammation, and osteoarthritis progression, and highlight the utility of gnotobiotic mouse models in dissecting microbiome-AhR interactions. Finally, we examine the therapeutic potential of AhR modulation in joint disease, emphasizing its relevance as a pharmaceutical target for osteoarthritis and age-related musculoskeletal decline.},
}

@article {pmid41903849,
year = {2026},
author = {Ekhlas, D and Verbiest, A and Stas, M and De Meyere, L and Vandermeulen, G and Tóth, J and Geboers, K and Timmermans, L and Verspecht, C and Wauters, L and Vermeersch, P and Jeppesen, PB and Verbeke, K and Joly, F and Derrien, M and Raes, J and Vanuytsel, T},
title = {Early ecological changes in intestinal microbiota with the long-acting GLP-2 analog apraglutide in short bowel syndrome.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {103138},
doi = {10.1016/j.clnesp.2026.103138},
pmid = {41903849},
issn = {2405-4577},
abstract = {BACKGROUND AND AIMS: Short bowel syndrome with intestinal failure (SBS-IF) is a rare, severe organ failure condition requiring long-term parenteral support. In SBS with colon-in-continuity (CiC), rapid transit and increased oxygen reshape gut and microbiota. We aimed to elucidate the effects of apraglutide, a novel long-acting glucagon-like peptide-2 (GLP-2) analogs, on the gut microbiome in SBS-IF-CiC.

METHODS: We performed a 52-week multicenter, open-label, phase 2 study in adults with SBS-IF-CiC (Leuven n = 7, Paris n = 2) receiving weekly subcutaneous apraglutide. Duodenal, distal small bowel and sigmoid colon biopsies, fecal- and plasma samples were collected over time. Analyses included mucosa-associated and fecal microbiota, fecal parameters, and fermentation metabolites. For baseline comparison, duodenal and sigmoid colonic biopsies from 20 controls (10 per region) were collected.

RESULTS: Patients exhibited an altered ecosystem characterized by reduced richness, loss of colonic anaerobes and dominance of Lactobacillus and Bifidobacterium with larger inter-subject variability, lower pH, higher moisture, and lower microbial load compared to controls. Apraglutide did not change overall diversity or stool parameters, but reduced inter-subject variability in stool and sigmoid colon. Notably, Bifidobacterium decreased in both stool and sigmoid colon, whereas Prevotella increased in stool from some patients. Still, Lactobacillus remained dominant. Specific taxa correlated with fecal butyrate, propionate, and reduced distal colonic motility, indicating microbial metabolism may support boosted adaptation.

CONCLUSIONS: This study emphasizes that SBS-IF-CiC features an immature distal gut microbiota and apraglutide promotes early ecological maturation, suggesting that combining GLP-2 analogs therapy with microbiome-targeted strategies may further enhance intestinal and ecosystem adaptation; ClinicalTrials.gov, Number NCT04964986https://www.

CLINICALTRIALS: gov/study/NCT04964986?term=NCT04964986&rank=1.},
}

@article {pmid41903990,
year = {2026},
author = {Gorji, L and Seldomridge, AN and Holder, AM},
title = {Leveraging the Human Microbiome to Improve Immunotherapy Sensitivity.},
journal = {Surgical oncology clinics of North America},
volume = {35},
number = {2},
pages = {285-298},
doi = {10.1016/j.soc.2025.10.007},
pmid = {41903990},
issn = {1558-5042},
mesh = {Humans ; *Immunotherapy/methods ; *Neoplasms/therapy/immunology/microbiology ; *Microbiota/immunology ; *Precision Medicine/methods ; Tumor Microenvironment/immunology ; },
abstract = {The human microbiome is composed of distinct microbial communities or ecosystems found throughout the human body, including within unique tumor microenvironments. In this review, we discuss the microbiome's influence on solid tumors, how the microbiome can be modulated to improve response to immunotherapy, and how emerging evidence suggests that microbiome modulation can add to the repertoire of personalized medicine.},
}

Humans
*Immunotherapy/methods
*Neoplasms/therapy/immunology/microbiology
*Microbiota/immunology
*Precision Medicine/methods
Tumor Microenvironment/immunology

@article {pmid41904117,
year = {2026},
author = {Chouhan, D and Grossman, AS and Kerns, KA and Stocke, KS and Kim, M and Dong, PT and Kumar, A and Lei, L and Lamont, RJ and McLean, JS and He, X and Bor, B},
title = {Ultrasmall oral Saccharibacteria modulate gingival immunoactivation through type IV pili and TLR2-dependent endocytosis.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-70546-5},
pmid = {41904117},
issn = {2041-1723},
support = {1R01DE031274//U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR)/ ; T90 DE026110-07//U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR)/ ; 1S10OD034405-01//U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR)/ ; T90 DE026110-07//U.S. Department of Health & Human Services | NIH | National Institute of Dental and Craniofacial Research (NIDCR)/ ; },
abstract = {Saccharibacteria are ultrasmall episymbionts that require host-bacteria to grow. They are positively associated with inflammatory diseases within the human microbiome, yet their mechanisms for interacting with the human host and contributing to diseases remain unknown. This study investigated the tripartite interactions between Saccharibacteria (Nanosynbacter lyticus strain TM7x and other strains), their host/non-host-bacteria, and human oral gingival epithelial cells. Both host and non-host-bacteria strongly induce proinflammatory cytokines in epithelial cells, while Saccharibacteria alone elicits limited immune activation. Remarkably, Saccharibacteria dampened proinflammatory cytokine responses to host/non-host-bacteria during coinfection. Mechanistically, this effect results from Saccharibacteria-mediated clustering and endocytosis of surface TLR2 receptor, ultimately leading to reduce TLR2-mediated cytokine signalling. Sacchribacteria type IV pili appendages facilitate epithelial cell binding and subsequent immune dampening via direct interaction between pili adhesins and TLR2. High resolution imaging shows that Saccharibacteria are internalized by epithelial cells through caveolin-mediated endocytosis, subsequently colocalize with endosome markers, and eventually are trafficked to lysosomes for degradation. Moreover, a subset of the Saccharibacteria survives lysosomal degradation and retains the ability to reinfect host-bacteria, highlighting a mechanism for transient persistence in the oral microbiome and a vital role in human immune and microbiome modulation.},
}

@article {pmid41904277,
year = {2026},
author = {M Davidson, I and Nikbakht, E and M O'Neill, H and Haupt, LM and Dunn, PJ},
title = {Shaping the Female Microbiome: A Review of Lifestyle Factors Influencing the Vaginal, Gut, Oral, and Skin Microenvironments.},
journal = {Microbial ecology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00248-026-02747-w},
pmid = {41904277},
issn = {1432-184X},
abstract = {The female microbiome, spanning the vaginal, gut, oral, and skin sites, harbours distinct microbial communities. Although the diversity and function of microbial communities across these sites are becoming increasingly understood, the extent to which modifiable lifestyle and environmental factors such as smoking, diet, alcohol intake, obesity, physical activity, stress, hygiene, and sexual behaviours shape these microbiomes remains underexplored. This review is restricted to modifiable lifestyle and environmental factors and does not comprehensively assess pharmaceutical exposures (e.g., antibiotics or hormonal therapies) or hormonal influence. To date, no review has comprehensively assessed and compiled evidence across the four microbial sites in females, despite their unique hormonal, physiological, and reproductive characteristics that distinctly influence microbial composition and function. This review provides a comprehensive examination of how such factors influence the dynamics of microbial composition and function along with site-specificity while also assessing cross-site microbial interactions. We focus exclusively on females to address a critical knowledge gap to provide a foundation from which future research and interventions can be tailored to women's health. This review discusses the underlying mechanisms driving microbial shifts and their impact on host health, highlighting critical gaps in our current knowledge. The integration of findings from multi-site microbiome research, highlights the potential to inform targeted, preventative, and therapeutic strategies that utilise the inherent dynamic nature of the microbiome to improve health outcomes across the female lifespan.},
}

@article {pmid41904418,
year = {2026},
author = {Kousar, R and Latif, S and Zahoor, M and Tabassum, S},
title = {A pilot study revealed the gut microbiota based on 16S rRNA metagenomics in gestational diabetes.},
journal = {BMC genomic data},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12863-026-01413-x},
pmid = {41904418},
issn = {2730-6844},
}

@article {pmid41904606,
year = {2026},
author = {Birkeland, S and Rohde Mæhlum, I and Senneset, M and Wik Taxerås, I and Snipen, L and Markov Arnesen, H and Boysen, P and Carlsen, H},
title = {A naturalized gut microbiome interacts with dietary fibers to protect against colonic inflammation.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2649435},
doi = {10.1080/19490976.2026.2649435},
pmid = {41904606},
issn = {1949-0984},
mesh = {Animals ; *Dietary Fiber/metabolism/administration & dosage ; *Gastrointestinal Microbiome ; Mice ; *Colitis/prevention & control/microbiology/chemically induced ; Feces/microbiology ; Dextran Sulfate ; Colon/microbiology/pathology ; Mice, Inbred C57BL ; Bacteria/classification/genetics/isolation & purification/metabolism ; Male ; Disease Models, Animal ; Intestinal Mucosa/metabolism/microbiology ; },
abstract = {"Feralized" mice, housed in farmyard-type environments, show a matured immunophenotype, altered intestinal barrier, and a shifted gut microbiome compared to conventionally housed laboratory mice. Since dietary fibers support gut health in part by microbial fermentation into immunomodulatory short-chain fatty acids, we hypothesized that feralization influences the intestinal barrier by enhancing the fiber-degrading properties of the microbiome. We explored whether susceptibility to low-grade dextran sulfate sodium-induced colitis differed between feralized and clean laboratory mice fed diets high or low in fermentable fibers. Feralized mice were protected against colitis, displaying low disease scores and biomarkers of inflammation in feces, plasma, and liver; and altered colonic mucosal gene expression, compared to clean mice. This protection was strongest with a fiber-rich diet, which, in contrast, worsened colitis in clean mice. Transfer of fecal microbiota from feralized mice to clean recipients conferred colitis protection. Fecal metagenome-assembled genomes revealed that the fiber-rich diet enriched the microbiome with predicted genes encoding fiber-degrading enzymes, while the low-fiber diet promoted mucin-degrading enzyme genes. However, the dominant microbial species contributing to these functions differed between feralized and laboratory mice. Differential abundance of bacterial taxa in feralized and laboratory mice further identified potential microbial modulators of colitis that merit targeted investigation in future studies. Overall, these findings suggest that fibers affect intestinal inflammation in a microbiota-dependent manner, underscoring the complex interplay between diet and microbiota in disease development.},
}

Animals
*Dietary Fiber/metabolism/administration & dosage
*Gastrointestinal Microbiome
Mice
*Colitis/prevention & control/microbiology/chemically induced
Feces/microbiology
Dextran Sulfate
Colon/microbiology/pathology
Mice, Inbred C57BL
Bacteria/classification/genetics/isolation & purification/metabolism
Male
Disease Models, Animal
Intestinal Mucosa/metabolism/microbiology

@article {pmid41904644,
year = {2026},
author = {Wang, W and Wen, Y},
title = {The role of systemic inflammation in hepatic encephalopathy: advances in inflammatory mechanisms, prevention and treatment research.},
journal = {Annals of medicine},
volume = {58},
number = {1},
pages = {2650232},
doi = {10.1080/07853890.2026.2650232},
pmid = {41904644},
issn = {1365-2060},
mesh = {*Hepatic Encephalopathy/therapy/etiology/prevention & control/immunology ; Humans ; Gastrointestinal Microbiome/immunology ; *Inflammation/complications/therapy/immunology ; Ammonia/metabolism ; Animals ; Dysbiosis/complications ; Fecal Microbiota Transplantation/methods ; Liver Cirrhosis/complications ; Hyperammonemia ; Rifaximin/therapeutic use ; Blood-Brain Barrier ; },
abstract = {OBJECTIVES: This review synthesizes current evidence establishing systemic inflammation as a key pathogenic driver in hepatic encephalopathy (HE) beyond hyperammonemia. It does not replace the ammonia hypothesis but rather acts as a critical synergistic factor, modulating and amplifying ammonia neurotoxicity. It further evaluates the mechanisms linking inflammation to HE and the therapeutic advances in inflammation-targeted prevention and treatment strategies.

METHODS: A comprehensive narrative literature review was conducted, analyzing relevant preclinical models and clinical studies. The search and synthesis focused on inflammatory mechanisms in chronic liver disease, gut-liver-brain axis dysfunction, cirrhosis-associated immune dysfunction (CAID), and resulting neuroinflammatory pathways.

RESULTS: Systemic inflammation, driven by gut dysbiosis, barrier failure, and CAID, amplifies ammonia neurotoxicity and independently contributes to neuroinflammation, blood-brain barrier disruption, and cerebral metabolic dysfunction in HE. Key inflammatory markers, such as IL-6, correlate with disease severity. Therapies targeting inflammation - particularly gut microbiota modulation with rifaximin and fecal microbiota transplantation (FMT) - demonstrate significant efficacy in reducing HE recurrence, lowering systemic inflammation, and improving cognitive outcomes. Other approaches, including albumin infusion, also show promise.

CONCLUSIONS: Systemic inflammation is a pivotal and synergistic factor in HE pathogenesis. Combining anti-inflammatory strategies that target the gut-liver-brain axis with traditional ammonia-lowering therapies offers a more comprehensive and effective treatment paradigm. Future research should prioritize protocol optimization, long-term safety assessment, and the development of personalized treatment approaches.},
}

*Hepatic Encephalopathy/therapy/etiology/prevention & control/immunology
Humans
Gastrointestinal Microbiome/immunology
*Inflammation/complications/therapy/immunology
Ammonia/metabolism
Animals
Dysbiosis/complications
Fecal Microbiota Transplantation/methods
Liver Cirrhosis/complications
Hyperammonemia
Rifaximin/therapeutic use
Blood-Brain Barrier

@article {pmid41904966,
year = {2026},
author = {Sun, H and Longdon, B and Raymond, B},
title = {Effect of the microbiome on pathogen susceptibility across four Drosophilidae species.},
journal = {Insect science},
volume = {},
number = {},
pages = {},
doi = {10.1111/1744-7917.70275},
pmid = {41904966},
issn = {1744-7917},
support = {NE/V012053/1//Natural Environment Research Council/ ; BB/K003240/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BB/S002928//BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; 109356/Z/15/Z/WT_/Wellcome Trust/United Kingdom ; WT097835MF/WT_/Wellcome Trust/United Kingdom ; WT101650MA/WT_/Wellcome Trust/United Kingdom ; //China Scholarship Council and University of Exeter PhD Scholarships/ ; },
abstract = {Microbiome have been shown to play an important role in host susceptibility to infections in some hosts. However, less is known about whether microbiota-mediated effects are consistent across host species, as our understanding of such interactions may be affected by publication bias. Following on from a large study of 36 species of Drosophilidae challenged with four bacterial pathogens, we identified two candidate host species that might have protective microbiomes based on low susceptibility and high abundance of culturable microbiota; we selected two other host species for comparison. We tested whether germ-reduced flies, and flies with natural or re-constituted microbiomes varied in their susceptibility to systemic infection with two bacterial pathogens (Providencia rettgeri and Staphylococcus aureus) and one viral pathogen (Drosophila C Virus). The composition and abundance of the bacterial microbiota varied between host species and microbiome treatments. We found an overall interaction between host species and pathogen type, confirming previous work that host species vary in their susceptibility in a pathogen specific manner. Similarly, we found that microbiome treatments had differing effects on host survival among host species, although some effect sizes tended to be small. In D. putrida individuals with manipulated microbiomes showed increased susceptibility to all pathogens tested; in other hosts altered susceptibility was pathogen dependent. While there are always challenges to manipulating microbiomes, especially across multiple host species, our results indicate that host microbiota play limited roles on survival in systemic infection in these four species. This work demonstrates that caution is required when generalizing about potential beneficial impact of microbiomes.},
}

@article {pmid41905017,
year = {2026},
author = {Gao, D and Hu, D and Xu, H and Li, X},
title = {A phage cocktail targeting multiple receptors reduces Salmonella Enteritidis colonization in chicks and modulates the cecal microbiome.},
journal = {Veterinary microbiology},
volume = {316},
number = {},
pages = {110999},
doi = {10.1016/j.vetmic.2026.110999},
pmid = {41905017},
issn = {1873-2542},
abstract = {Salmonella Enteritidis is a major pathogen responsible for foodborne illnesses, frequently causing public health issues through the contamination of poultry products and posing a serious threat to the poultry industry. In recent years, phages have emerged as a promising alternative to antibiotics for prevention and control strategies. In this study, a rationally designed phage cocktail from previous research was used, consisting of four phages targeting different receptors: GSP162, GSP193, GSP001, and GSP032. An infection model of chicks infected with S. Enteritidis strain SE006 was established to systematically assess the in vivo protective effects of the phage cocktail. The results demonstrated that the phage cocktail reached high concentrations in the chick ceca and showed a trend toward reduction in the ceca load of S. Enteritidis. In the phage-treated group, the cecal S. Enteritidis load was reduced by an average of 0.75 ± 0.34 log10 CFU/g on day 1 and 1.01 ± 0.33 log10 CFU/g on day 4 post-treatment, respectively. Gut microbiota analysis revealed that the phage cocktail modulated the dysbiosis induced by S. Enteritidis SE006 infection and facilitated the establishment of the early cecal microbial community in chicks. This study provides preliminary experimental evidence supporting the potential of phage-based biocontrol of Salmonella in poultry, laying a foundation for further field validation in commercial settings before practical application.},
}

@article {pmid41905051,
year = {2026},
author = {Nguyen, TD and Huang, YC and Zhang, S and Itayama, T and Mo, J and Liu, X and Liu, W and Wang, Z},
title = {Sex-specific gut microbiota dysbiosis and intergenerational effects of florfenicol in Tigriopus japonicus: Maternal-only or biparental contributions?.},
journal = {Journal of hazardous materials},
volume = {508},
number = {},
pages = {141871},
doi = {10.1016/j.jhazmat.2026.141871},
pmid = {41905051},
issn = {1873-3336},
abstract = {Florfenicol, an antibiotic widely used in mariculture, raises concerns about long‑term impacts on non‑target marine organisms. However, its intergenerational effects and underlying mechanisms remain poorly understood. We exposed marine copepods (Tigriopus japonicus) to florfenicol in acute assays and chronically exposed the parental generation (F0) to environmentally detected concentrations, followed by a cross‑mating design to evaluate effects in unexposed offspring (F1). Acute exposure caused no naupliar mortality after 96 h, although copepodite swimming activity declined significantly at ≥ 25 mg/L, indicating limited direct toxicity under short‑term exposure. In contrast, chronic F0 exposure delayed metamorphosis, skewed sex ratios toward females, and unexpectedly increased fertility. In F1, developmental delay persisted when either both parents or only mothers were exposed, suggesting a trade‑off between reproductive output and developmental pace. The female‑based sex ratio also carried over, with contributions from both maternal and paternal exposure. Gut microbiome dysbiosis occurred in both sexes but was sex‑specific, characterized by reduced beneficial taxa (e.g., Lactobacillus) and enrichment of opportunistic, antibiotic‑resistant Acinetobacter, particularly following maternal exposure. This study provides the first evidence that parental, sex‑specific microbiome disruption mediates intergenerational antibiotic effects, highlighting dominant maternal influences while also implicating paternal roles. Validation across taxa, broader antibiotic assessments, and targeted molecular investigations are needed to confirm these patterns and elucidate further underlying pathways. Overall, our findings underscore the ecological risks of florfenicol contamination in mariculture zones and emphasize the importance of incorporating parental and intergenerational responses into ecotoxicological assessments.},
}

@article {pmid41905316,
year = {2026},
author = {Young-Yusty, S and Prescilla-Ledezma, A and Acosta-de Patiño, H},
title = {Diversity and antibiotic resistance profiles of bacteria isolated from the oral cavity of captive snakes.},
journal = {Revista Argentina de microbiologia},
volume = {58},
number = {3},
pages = {100711},
doi = {10.1016/j.ram.2026.100711},
pmid = {41905316},
issn = {0325-7541},
abstract = {Venomous snake bites are a global public health issue, causing between 81000 and 138000 annual deaths and 400000 permanent disabilities. This study investigated the oral bacterial diversity and antibiotic resistance profiles in captive Viperidae snakes. Oral swabs from 48 specimens across four species (Porthidium lansbergii, Bothriechis nigroviridis, Cerrophidion sasai, and Bothrops asper) were analyzed using culture-dependent methods. Bacterial isolation and identification using the VITEK 2 automated system revealed 41 strains from 12 genera, predominantly Gram-negative bacteria, including Morganella morganii (11 isolates) and Providencia rettgeri (10 isolates). Antibiotic susceptibility testing demonstrated significant resistance patterns, with 100% resistance to cephalothin and cefazolin in M. morganii, and emerging extended-spectrum β-lactamase (ESBL) production in Enterobacter cloacae and Sphingomonas paucimobilis. The comparative analysis showed that P. lansbergii exhibited the highest bacterial diversity. These findings highlight the complex oral microbiota of venomous snakes and underscore the need for evidence-based antibiotic strategies in snakebite management, particularly given the global rise in antimicrobial resistance.},
}

@article {pmid41905324,
year = {2026},
author = {Chalif, J and Moruzzi, C and Velasquez, J and O'Connor, R and Fulton, J and Mehra, Y and Cohn, DE and Copeland, LJ and Cosgrove, CM and Nagel, CI and O'Malley, DM and Monovich, L and Spakowicz, DJ and Chambers, LM},
title = {Implementing non-invasive biospecimen collection in gynecologic oncology: Insights from a prospective gut microbiome feasibility study.},
journal = {Gynecologic oncology},
volume = {208},
number = {},
pages = {63-68},
doi = {10.1016/j.ygyno.2026.03.008},
pmid = {41905324},
issn = {1095-6859},
abstract = {OBJECTIVE(S): The gut microbiome is increasingly recognized as an important modulator of treatment response and other outcomes in gynecologic cancers, but data are limited regarding the logistics of incorporating stool sample collection into clinical practice. We evaluated the feasibility of integrating non-invasive stool biospecimen collection into routine gynecologic oncology care, described recruitment and compliance, and identified factors associated with participation.

METHODS: This prospective, single-institution study was conducted from March 2023 to April 2024. Eligible gynecologic oncology patients were approached for Total Cancer Care® enrollment and offered participation in an optional linked stool biospecimen substudy. Patients who consented received an at-home stool collection kit. Clinical and demographic data were abstracted from the electronic medical record, and multivariable logistic regression identified predictors of Total Cancer Care enrollment, stool kit acceptance, and stool kit return.

RESULTS: A total of 666 patients were approached, of whom 407 (61%) enrolled in Total Cancer Care. Among enrollees, 234 (58%) accepted a stool kit, and 100 (43%) of those who accepted returned a completed sample. On multivariable analysis, prior clinical trial participation (p < 0.01) and provider (p < 0.05) were independently associated with Total Cancer Care enrollment. Stool kit acceptance was most strongly predicted by treating provider (p < 0.0001). No demographic or clinical variables were significantly associated with kit return.

CONCLUSION(S): Implementation of an at-home stool collection program in gynecologic oncology is feasible. Provider engagement was the strongest determinant of acceptance. These findings provide real-world benchmarks for recruitment and compliance and establish a foundation for future microbiome-focused translational studies.},
}

@article {pmid41905328,
year = {2026},
author = {Matheoud, D and Akbar, I and Hercun, J and Stratton, JA},
title = {A liver-mitochondria-immune axis in Parkinson's disease: emerging perspectives on a hepatic origin for mitochondrial autoimmunity as a driver of Parkinson's disease.},
journal = {Current opinion in immunology},
volume = {100},
number = {},
pages = {102761},
doi = {10.1016/j.coi.2026.102761},
pmid = {41905328},
issn = {1879-0372},
abstract = {Parkinson's disease (PD) is increasingly understood as a systemic disorder with early manifestations outside the central nervous system. Converging clinical, metabolic, and immunological observations highlight overlaps between PD and primary biliary cholangitis (PBC), a prototypic autoimmune cholestatic liver disease. A shared hallmark of both conditions is mitochondrial dysfunction and immune dysregulation, particularly in the context of bile acid (BA) metabolism. In this Current Opinion-style perspective, we integrate recent advances in microbiome biology, BA signaling, and mitochondrial antigen presentation to propose that hepatic stress may contribute to PD pathogenesis by promoting immune exposure to mitochondrial antigens, a proautoimmune cytokine environment, and the generation of mitochondrial‑reactive cytotoxic T cell responses. We discuss how alterations in BA and the promotion of dysbiosis - documented in both PBC and PD - can induce ductular reaction, immunogenic apoptosis, and MitAP, thereby providing a mechanistic bridge between liver inflammation and adaptive immunity. Despite divergent clinical presentations, PBC and PD may share critical upstream pathways linking hepatic metabolism, mitochondrial antigenicity, and immune tolerance. We argue that further investigation of a liver-mitochondria-immune axis may yield new insights into PD initiation and progression.},
}