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24 pages, 3654 KB

Open AccessArticle

High Humidity Exacerbates Rheumatoid Arthritis in Mice via Prevotella stercorea-Mediated Chondroitin Sulfate Degradation

by Mingzhu Wang, Qianqian He, Yiwu Qiu, Lin Huang, Yun Zhang, Ding Ye, Zhixing He and Chengping Wen

Microorganisms 2026, 14(7), 1540; https://doi.org/10.3390/microorganisms14071540 - 14 Jul 2026

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Abstract

Background: Rheumatoid arthritis (RA) is influenced by environmental exposures. High humidity has been clinically associated with worsened joint symptoms, but the microbial and metabolic mechanisms remain unclear. We investigated whether a gut microbiota–metabolism axis contributes to humidity-associated aggravation of collagen-induced arthritis (CIA). Methods: [...] Read more.

Background: Rheumatoid arthritis (RA) is influenced by environmental exposures. High humidity has been clinically associated with worsened joint symptoms, but the microbial and metabolic mechanisms remain unclear. We investigated whether a gut microbiota–metabolism axis contributes to humidity-associated aggravation of collagen-induced arthritis (CIA). Methods: CIA mice were maintained under normal or high relative humidity. We integrated 16S rRNA and metagenomic sequencing, liquid chromatography–tandem mass spectrometry metabolomics, and intestinal barrier assessments. Fecal microbiota transplantation (FMT) was performed to evaluate microbiota dependency. Based on multi-omics findings, we quantified chondroitin sulfate (CS) and conducted functional experiments involving Prevotella stercorea (P. stercorea) supplementation, CS administration, and in vitro degradation assays. Results: High humidity aggravated arthritis severity and systemic inflammation, including increased interleukin-6, interleukin-17A, and granulocyte colony-stimulating factor, and was accompanied by impaired intestinal barrier integrity. FMT supported a microbiota-dependent contribution. Metagenomic analysis identified enrichment of P. stercorea and glycosaminoglycan degradation pathways under high humidity. CS abundance was reduced in articular cartilage, P. stercorea degraded CS in vitro and was associated with cartilage CS loss in vivo, and CS supplementation attenuated arthritis under high humidity and reduced the arthritis-promoting effects associated with P. stercorea. Conclusions: High humidity is associated with microbiota-dependent functional remodeling, enhanced CS degradation, and aggravated arthritis in CIA mice. These findings suggest that humidity-associated alterations in microbial CS metabolism may link environmental exposure to cartilage disruption and joint inflammation. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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14 pages, 3263 KB

Open AccessArticle

Black Soldier Fly Larvae Bioconvert Deoxynivalenol-Contaminated Feed Without Toxin Accumulation: Growth Performance, Residue Distribution, and Gut Microbiota Responses

by Kun Liu, Yuting Li, Minghui Jiao, Jianlai Guo, Xiangbo Ji, Huibin Shi, Jun Li, Weixian Zhang, Kai Quan, Zhentian Li and Xilan Jiao

Microorganisms 2026, 14(7), 1452; https://doi.org/10.3390/microorganisms14071452 - 1 Jul 2026

Cited by 1 | Viewed by 398

Abstract

Deoxynivalenol (DON) contamination poses a major threat to feed safety and animal health, yet safe and sustainable strategies for managing DON-contaminated feed remain limited. Black soldier fly larvae (BSFL) have shown strong tolerance to various mycotoxin-contaminated substrates and generally exhibit limited toxin bioaccumulation, [...] Read more.

Deoxynivalenol (DON) contamination poses a major threat to feed safety and animal health, yet safe and sustainable strategies for managing DON-contaminated feed remain limited. Black soldier fly larvae (BSFL) have shown strong tolerance to various mycotoxin-contaminated substrates and generally exhibit limited toxin bioaccumulation, making them a promising biological system for the valorization of contaminated organic resources. This study evaluated the effects of DON-contaminated feed on BSFL growth performance, bioconversion efficiency, DON residue distribution, and gut microbial responses. Results showed that DON exposure had no significant effect on larval survival, body length, or body weight, nor on the efficiency of conversion of digested feed, substrate reduction rate, or waste reduction index. Residue analysis showed that DON was below the limit of detection in larval samples after BSFL treatment, while the DON concentration in frass was approximately 81.10% lower than that in the initial substrate, indicating no detectable in vivo bioaccumulation. Gut microbiota analysis showed no significant changes in alpha diversity, with minor compositional trends in specific taxa. Firmicutes remained the predominant phylum, whereas Actinobacteriota increased. These findings provide new insights into host–microbe adaptations under mycotoxin stress and support further evaluation of BSFL-based strategies for managing DON-contaminated feed resources. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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20 pages, 8303 KB

Open AccessArticle

Salmonella Effector SpvC Targets SEC23B of Intestinal Epithelial Cells to Resist Gasdermin D-Mediated Protection Against Systemic Infection

by Liting Zhou, Yan Yang, Li Kang, Jiayi You, Ye Wang, Ailing Xu, Guangmin Tu, Rui Huang, Zhengyu Zhou, Minghui Li and Shuyan Wu

Microorganisms 2026, 14(5), 1148; https://doi.org/10.3390/microorganisms14051148 - 19 May 2026

Cited by 1 | Viewed by 422

Abstract

Salmonella infects a wide range of hosts, causing gastroenteritis or systemic infection in humans and animals, highlighting the urgent need for a deeper understanding of its pathogenesis. SpvC, a critical virulence determinant of salmonella, facilitates bacterial dissemination. Gasdermin D (GSDMD) is the only [...] Read more.

Salmonella infects a wide range of hosts, causing gastroenteritis or systemic infection in humans and animals, highlighting the urgent need for a deeper understanding of its pathogenesis. SpvC, a critical virulence determinant of salmonella, facilitates bacterial dissemination. Gasdermin D (GSDMD) is the only gasdermin known to protect mice against acute Salmonella enteritis. Our preliminary findings indicated that SpvC counteracts GSDMD-mediated antibacterial effects to enhance bacterial dissemination, although its functional relevance to epithelial-derived GSDMD and the underlying mechanisms remain unclear. To address this, Gsdmd^−/− C57BL/6J and wild-type mice were infected with Salmonella Typhimurium (S. Typhimurium) wild-type strain and spvC deletion mutant. Our results demonstrate that SpvC compromises intestinal epithelial barrier integrity, overcoming GSDMD-mediated protection against systemic infection. Specifically, through bioinformatics analysis, LC-MS/MS, and in vivo experiments with Caco-2 cell monolayers and site-directed spvC mutants, we identified SEC23B as a novel target of SpvC. This interaction disrupts the intestinal epithelial barrier through the autophagy–pyroptosis pathway. This study identifies SEC23B as a unique cellular target of SpvC involved in GSDMD activation during S. Typhimurium systemic infection. It also reveals a novel mechanism by which Salmonella evades host defense mechanisms. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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28 pages, 19843 KB

Open AccessArticle

Functional Shifts in Gut Microbiota and Associated Metabolites Suggest Gut–Brain Axis Dysregulation in Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS)

by Shabana M. Shaik, Gabriele Schiro, Daniel Laubitz, Juliette C. Madan, Connor P. Kelley, Michael Daines, Sydney A. Rice, Fayez K. Ghishan and Pawel R. Kiela

Microorganisms 2026, 14(5), 1036; https://doi.org/10.3390/microorganisms14051036 - 2 May 2026

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Abstract

Background: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS) are characterized by neuropsychiatric symptoms linked to immune dysregulation. Emerging evidence highlights the role of host–microbiome interactions in modulating neuro-immune functions via gut–brain axis signaling; however, its contribution to PANDAS pathophysiology remains poorly [...] Read more.

Background: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS) are characterized by neuropsychiatric symptoms linked to immune dysregulation. Emerging evidence highlights the role of host–microbiome interactions in modulating neuro-immune functions via gut–brain axis signaling; however, its contribution to PANDAS pathophysiology remains poorly understood. Methods: We conducted microbiome analysis from samples collected across multiple sites of PANDAS patients including nasal, throat and stool. We performed an integrated multi-omics analysis of stool samples from pediatric PANDAS cases and healthy controls, including discordant twin pairs. Microbial composition and function were assessed using 16S rRNA gene sequencing, shotgun metagenomics, while untargeted metabolomic profiling was performed using ultra-performance liquid chromatography-mass spectrometry (UPLC-MS/MS). Results: PANDAS cases exhibited reduced alpha diversity and significantly altered beta diversity compared to controls, indicating shifts in gut microbial composition. Shotgun metagenomic analysis revealed differential enrichment of functional pathways, including diminished quorum sensing, altered gamma-aminobutyric acid (GABA) biosynthesis, and microbial degradation processes. Multiple gut–brain modules (GBMs) and gut metabolic modules (GMMs) associated with neurotransmission, transport activities and metabolism were significantly perturbed in PANDAS. Metabolomic profiling showed reduced functional diversity and distinct clustering of metabolic profiles, with differential abundance of amino acids, bile acids, and neuroactive compounds. Integrative analysis further identified disrupted microbe–metabolite networks allied to gut–brain signaling. Conclusions: Our findings reveal significant functional shifts in gut microbiota composition, functional capacity and metabolite profile in PANDAS, suggesting dysregulation of the gut–brain axis signaling. This study provides a foundation for development of microbiome-based biomarkers and therapeutic strategies for pediatric neuropsychiatric disorders. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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26 pages, 15038 KB

Open AccessArticle

Akkermansia muciniphila NND9 Mitigates Ulcerative Colitis by Ameliorating the Gut Barrier via Suppressing DR5 Expression in a Mouse Model

by Xin-Yu Gao, Yan Wang, Yu-Hui Wang, Hao Yu, Liang Liu, Xing-Hua Zhang, Hong-Tao Xu, Yao Meng, Randal N. Johnston, Gui-Rong Liu and Shu-Lin Liu

Microorganisms 2026, 14(5), 1002; https://doi.org/10.3390/microorganisms14051002 - 29 Apr 2026

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Abstract

Ulcerative colitis (UC) is a type of inflammatory bowel disease without curative therapeutics. Recent studies demonstrate that Akkermansia muciniphila exerts mitigating effects on UC, but the underlying mechanisms remain unclear. In this study, we isolated a strain of A. muciniphila, designated NND9, [...] Read more.

Ulcerative colitis (UC) is a type of inflammatory bowel disease without curative therapeutics. Recent studies demonstrate that Akkermansia muciniphila exerts mitigating effects on UC, but the underlying mechanisms remain unclear. In this study, we isolated a strain of A. muciniphila, designated NND9, from the feces of DSS-induced ulcerative colitis model mice and investigated its effects on UC of the mouse model. NND9 significantly alleviated UC severity in the mice by restoring gut barrier integrity through improving colonic mucus layer thickness, mitigating goblet cell depletion, and halting epithelial cell death. Mechanistically, NND9 suppressed the expression of the Tnfrsf10b gene encoding death receptor 5 (DR5) on the surface of colonic epithelial cells. Additionally, NND9 inhibited the phosphorylation of kinase 3 (RIPK3) and the pseudokinase mixed-lineage kinase domain-like protein (MLKL) associated with the necrotic apoptosis pathway, thereby reducing gut epithelial cell death. NND9 also markedly ameliorated the gut microbiome of the colitis mice. Untargeted metabolomics analysis demonstrated that NND9 modulated both tryptophan and bile acid metabolism. In conclusion, NND9 exhibits curative effects on UC by resolving inflammatory reactions of the gut mucosa through the DR5-RIPK3/p-RIPK3-MLKL/p-MLKL pathway and redressing gut dysbiosis. This study provides valuable information for the development of innovative therapeutic strategies for the treatment of UC. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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16 pages, 2329 KB

Open AccessArticle

Microbial Biomarkers for the Prevention and Diagnosis of Alcoholic Liver Disease

by Goo Hyun Kwon, Hyunjoon Park, Hyeong Seop Kim, Ki Kwang Oh, Jung A Eom, Kyeong Jin Lee, Min Ju Kim, Minsoo Kim, Jeong Su Kim, Sang Hak Han, Young Lim Ham and Ki Tae Suk

Microorganisms 2026, 14(2), 449; https://doi.org/10.3390/microorganisms14020449 - 12 Feb 2026

Cited by 1 | Viewed by 1201

Abstract

Alterations in gut microbiota are closely associated with alcohol-associated liver disease (ALD) progression. We aimed to identify ALD-related bacterial strains with therapeutic or diagnostic potential. Human fecal samples were analyzed to screen candidate microbes, and an ALD mouse model was used to evaluate [...] Read more.

Alterations in gut microbiota are closely associated with alcohol-associated liver disease (ALD) progression. We aimed to identify ALD-related bacterial strains with therapeutic or diagnostic potential. Human fecal samples were analyzed to screen candidate microbes, and an ALD mouse model was used to evaluate their effects. We also assessed bacterial DNA levels in blood to explore diagnostic utility. Lactobacillus helveticus and L. lactis treatment improved gut dysbiosis and reduced hepatic inflammation and endotoxemia. In contrast, Veillonella dispar, which is significantly enriched in ALD patients, had no beneficial effects in vivo. Instead, V. dispar abundance in blood distinguished ALD patients from controls with an area under the ROC curve of 0.815. These findings suggest that L. helveticus and L. lactis may be effective probiotics for ALD, while V. dispar may serve as a non-invasive diagnostic biomarker. Targeting microbiota may offer a new approach for ALD prevention and diagnosis. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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17 pages, 10285 KB

Open AccessArticle

Microcin C7 Prevents Cyclophosphamide-Induced Immunosuppression and Intestinal Injury by Modulating T-Cell Differentiation and Gut Microbiota Composition in Mice

by Jianfei Zhao, Zhongqian Lu, Jialin Wu, Li Wang, Jinxiu Huang and Feiyun Yang

Microorganisms 2026, 14(2), 350; https://doi.org/10.3390/microorganisms14020350 - 3 Feb 2026

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Abstract

Microcin C7 (McC7) is a ribosomally synthesized antimicrobial peptide that has emerged as a promising candidate due to its dual antibacterial and immunomodulatory activities. This study evaluated the preventive effect of McC7 against cyclophosphamide (CTX)-induced immunosuppression and intestinal injury. An immunosuppression model was [...] Read more.

Microcin C7 (McC7) is a ribosomally synthesized antimicrobial peptide that has emerged as a promising candidate due to its dual antibacterial and immunomodulatory activities. This study evaluated the preventive effect of McC7 against cyclophosphamide (CTX)-induced immunosuppression and intestinal injury. An immunosuppression model was established by intraperitoneal CTX injection in mice, which were randomly allocated into five groups (n = 15): a negative control, a CTX model group, and three McC7 treatment groups receiving dietary McC7 at 100, 200, or 400 mg/kg both before and during CTX exposure. Body weight and feed intake were monitored throughout the study. Organ indices, serum biochemical parameters, immune and antioxidant markers, and intestinal morphology were assessed. Splenic T-cell subsets were analyzed by flow cytometry, and gut microbiota composition was evaluated by 16S rRNA sequencing. McC7 supplementation significantly attenuated the CTX-induced reduction in body weight, feed intake, and organ indices, ameliorated markers of hepatic and renal injury, and restored the splenic CD4⁺/CD8⁺ T-cell ratio. McC7 enhanced intestinal mucosal barrier integrity, increased the abundance of beneficial bacteria such as Candidatus Arthromitus and ASF356, and reduced the abundance of the potentially pathogenic genus Bilophila. In conclusion, our results demonstrate that McC7 alleviates CTX-induced immunosuppression by regulating T-cell differentiation, maintaining cytokine homeostasis, and modulating gut microbial composition to support intestinal health. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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Review

Jump to: Research

38 pages, 4578 KB

Open AccessReview

Nontoxigenic Bacteroides fragilis as a Next-Generation Probiotic: Mechanisms, Safety, and Therapeutic Potential

by Dong Wang, Zheng Nie, Wenzheng Zhang, Jinhui Liu, Changqi Ge, Yannan Zhang, Yabin Lu, Zhanhai Mai, Xiaodong He, Jianlong Li, Chao Gong and Qingyong Guo

Microorganisms 2026, 14(8), 1795; https://doi.org/10.3390/microorganisms14081795 - 14 Aug 2026

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Abstract

Nontoxigenic Bacteroides fragilis (NTBF) is defined by the absence of the bft gene and corresponding B. fragilis toxin production; however, nontoxigenic status alone does not establish uniform safety or probiotic function. This review critically evaluates strain-level biological characteristics, safety, mechanisms, metabolites, and disease-model [...] Read more.

Nontoxigenic Bacteroides fragilis (NTBF) is defined by the absence of the bft gene and corresponding B. fragilis toxin production; however, nontoxigenic status alone does not establish uniform safety or probiotic function. This review critically evaluates strain-level biological characteristics, safety, mechanisms, metabolites, and disease-model evidence. Selected strains and defined strain-derived preparations, including ZY-312, HCK-B3, NCTC 9343-derived polysaccharide A, and ZY-312-derived zwitterionic capsular polysaccharide preparation TP2, have shown immunomodulatory, barrier-associated, and microbial-community-modulating activities, predominantly in vitro and in animal models. Direct causal evidence is limited to specific strain–preparation–host–model combinations, whereas many changes in cytokines, tight-junction-associated proteins, microbial composition, and organic-acid profiles remain functional or associative. Protective effects have been reported in preclinical models of inflammatory bowel disease, necrotizing enterocolitis, antibiotic-associated diarrhea, Clostridioides difficile infection, and enterotoxigenic B. fragilis (ETBF)-associated tumorigenesis. However, findings are highly dependent on the strain, preparation, dose, administration timing, host, and model. Safety remains incompletely resolved because the absence of B. fragilis toxin (BFT) does not exclude opportunistic or systemic infection, antimicrobial-resistance mobility, bacterial translocation, permeability changes, or adverse effects during long-term administration. Metabolic effects may also be beneficial or adverse depending on the strain, host dietary and genetic background, and experimental context. Human evidence is primarily observational, and robust intervention trials are lacking. Accordingly, NTBF should be regarded as a heterogeneous group of strain-specific live-biotherapeutic candidates requiring rigorous strain-specific manufacturing, potency, dose, antimicrobial-susceptibility, and safety evaluation. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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14 pages, 568 KB

Open AccessReview

Probiotic Yeasts and Bacteria: A Complementary Approach to Gut Health

by Arrigo F. G. Cicero, Cecilia Bartoli, Carla Lluís-Ganella and Paolo Fabrizzi

Microorganisms 2026, 14(8), 1763; https://doi.org/10.3390/microorganisms14081763 - 11 Aug 2026

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Abstract

Probiotics are live microorganisms that, when administered in adequate amounts, confer a health benefit to the host. Research has traditionally focused on bacterial species, particularly Lacticaseibacillus and Bifidobacterium, whose mechanisms are well-characterised. However, probiotic yeasts represent a functionally distinct category, with Saccharomyces [...] Read more.

Probiotics are live microorganisms that, when administered in adequate amounts, confer a health benefit to the host. Research has traditionally focused on bacterial species, particularly Lacticaseibacillus and Bifidobacterium, whose mechanisms are well-characterised. However, probiotic yeasts represent a functionally distinct category, with Saccharomyces boulardii as the most studied representative and Kluyveromyces marxianus as an emerging candidate. Bacterial and yeast probiotics differ in cell biology, antibiotic susceptibility, immune receptor engagement, and metabolic output. Bacterial strains provide mucosal adhesion and direct short-chain fatty acid (SCFA) generation but are susceptible to antibacterial therapy. Yeast strains are intrinsically antibiotic-resistant, offer enzymatic activities such as β-galactosidase and glycosidases, and exert indirect bifidogenic effects that amplify luminal SCFA concentrations beyond what either category achieves alone. These non-overlapping profiles support a complementary rather than competitive conceptualisation of their use. When combined with prebiotic substrates such as fructooligosaccharides or galactooligosaccharides, this integrated approach addresses the principal axes of intestinal homeostasis more comprehensively than any single-organism intervention. Prospective randomised trials are needed to determine whether this mechanistic complementarity translates into additive or synergistic clinical benefit. This review synthesises the available evidence and proposes a framework for their complementary use. The proposed framework is hypothesis-generating: it rests largely on mechanistic and preclinical data, and its clinical validity requires confirmation in adequately powered controlled trials. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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17 pages, 8844 KB

Open AccessReview

Microbiota–Immune Crosstalk in Pneumonia and Acute Lung Injury: Mechanisms, Evidence, and Therapeutic Opportunities

by Haoran Yuan, Bingyi Li, Caihong Shen, Lixin Xie and Fei Hou

Microorganisms 2026, 14(8), 1758; https://doi.org/10.3390/microorganisms14081758 - 10 Aug 2026

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Abstract

Mucosal microbiota contribute broadly to host defense and immune homeostasis, while the lung and gut microbiota form a particularly important bidirectional ecological and immunological network that shapes pulmonary host defense, inflammatory injury, and tissue repair. In pneumonia, loss of colonization resistance and altered [...] Read more.

Mucosal microbiota contribute broadly to host defense and immune homeostasis, while the lung and gut microbiota form a particularly important bidirectional ecological and immunological network that shapes pulmonary host defense, inflammatory injury, and tissue repair. In pneumonia, loss of colonization resistance and altered microbial metabolite production may weaken innate and adaptive immunity; respiratory infection, antibiotics, and critical-care exposures can, in turn, remodel both microbial communities. In acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), intestinal barrier failure, circulating microbial products, immune cell trafficking and, in selected settings, lymphatic or hematogenous dissemination of gut-derived organisms may aggravate alveolar–capillary injury. Alveolar macrophages integrate these signals through pattern-recognition, metabolic, and epigenetic pathways, linking microbial ecology to pathogen clearance and inflammatory resolution. The evidence, however, remains uneven. Mechanistic causality rests largely on animal studies, most human data are associative, and trials of microbiota-directed interventions are heterogeneous and strain-specific. This Review examines bacterial and viral pneumonia, sepsis-associated ALI and ventilator-associated injury; separates mechanistic, observational, and interventional evidence; and evaluates probiotics, live biotherapeutic products, microbial metabolites, and dietary approaches. Translation will depend on longitudinal sampling, source-resolved microbial tracking, metabolite-informed patient stratification, and adequately powered trials with clinically relevant endpoints. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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26 pages, 938 KB

Open AccessReview

Restoring Microbial Balance: Clinical Applications, Challenges, and Future Directions of Fecal Microbiota Transplantation in Pediatric Disorders

by Giulia Zambelli, Marco Masetti, Sonia Rasmi, Irene Addati, Lorenzo Bonacorsi, Sonia Diona and Susanna Esposito

Microorganisms 2026, 14(6), 1241; https://doi.org/10.3390/microorganisms14061241 - 31 May 2026

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Abstract

Fecal microbiota transplantation (FMT) has emerged as a microbiota-directed therapeutic strategy with established efficacy in recurrent Clostridioides difficile infection (rCDI) and expanding investigational applications in pediatric medicine. Given the central role of the gut microbiota in immune maturation, metabolic homeostasis, and colonization resistance—particularly [...] Read more.

Fecal microbiota transplantation (FMT) has emerged as a microbiota-directed therapeutic strategy with established efficacy in recurrent Clostridioides difficile infection (rCDI) and expanding investigational applications in pediatric medicine. Given the central role of the gut microbiota in immune maturation, metabolic homeostasis, and colonization resistance—particularly during early life—restoring microbial diversity represents a biologically plausible intervention for disorders characterized by dysbiosis. This narrative review critically examines current evidence regarding the indications, efficacy, safety, and practical considerations of FMT in pediatric populations. A structured literature search was conducted across PubMed/MEDLINE, Scopus, Web of Science, and the Cochrane Library from inception through December 2025. Eligible studies included randomized controlled trials, observational studies, systematic reviews, meta-analyses, and guideline statements addressing pediatric FMT. RCDI remains the primary and best-supported indication, with reported success rates exceeding 80% after a single FMT and approaching 90% with repeat procedures. Evidence for other indications—including inflammatory bowel disease (IBD), malignancy-associated CDI, transplant recipients, multidrug-resistant organism (MDRO) decolonization, neurodevelopmental disorders, allergic colitis, and functional gastrointestinal disorders—remains limited and heterogeneous. While short-term remission rates in pediatric ulcerative colitis appear promising, data derive largely from small, non-standardized studies, and long-term efficacy and safety remain insufficiently defined. FMT usage in immunocompromised children, particularly oncology and transplant populations, is controversial due to limited pediatric-specific evidence and theoretical risks. Substantial variability in donor screening, preparation methods, dosing, and administration routes further limits standardization. Currently, FMT should be considered established therapy for pediatric rCDI, whereas other applications require well-designed, multicenter trials with long-term follow-up to clarify safety and clinical benefit. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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21 pages, 767 KB

Open AccessReview

Probiotics and Antibiotics: From Empirical Practice to a Biological Rationale for Targeted Choice During Antibiotic Therapy

by Mariarosaria Matera, Valentina Biagioli, Stefano Leo and Lorenzo Drago

Microorganisms 2026, 14(4), 763; https://doi.org/10.3390/microorganisms14040763 - 27 Mar 2026

Cited by 2 | Viewed by 2513

Abstract

Antibiotic therapy represents one of the strongest ecological perturbations of the human gut microbiota, inducing rapid and often prolonged alterations in community structure, metabolic activity, and functional resilience. While the use of probiotics to mitigate antibiotic-associated dysbiosis is widely adopted in clinical practice, [...] Read more.

Antibiotic therapy represents one of the strongest ecological perturbations of the human gut microbiota, inducing rapid and often prolonged alterations in community structure, metabolic activity, and functional resilience. While the use of probiotics to mitigate antibiotic-associated dysbiosis is widely adopted in clinical practice, probiotic selection is still largely empirical and insufficiently grounded in biological compatibility with specific antibiotic pressures. In this conceptual review, antibiotics are reframed not merely as antimicrobial agents, but as ecological forces that shape microbial survival, quiescence, and recolonization dynamics. We propose a biologically informed framework that distinguishes genetic antibiotic resistance from functional or ecological insensitivity, highlighting how microbial traits, such as the absence or inaccessibility of the antibiotic target, metabolic state, sporulation, and cellular architecture, influence the persistence of probiotics during antibiotic exposure. By integrating the mechanisms of action of antibiotics with key physiological and structural features of probiotic microorganisms, we develop a conceptual framework aimed at rationalizing the compatibility of probiotics and antibiotics. This framework does not imply clinical efficacy but provides an interpretative tool to guide hypothesis generation, experimental validation, and the design of future targeted probiotic strategies. A more ecologically grounded approach to probiotic selection may ultimately improve microbiota support during antibiotic therapy and advance personalized microbiome modulation. Full article

(This article belongs to the Special Issue Advances in Gut Microbiota–Host Interactions: Microbial Mechanisms, Modulators, and Translational Perspectives)

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