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Journal articleDecker V, Qureshi K, Roberts L, et al., 2025,
The emerging role of the gut microbiota in vaccination responses.
, Gut Microbes, Vol: 17The gut microbiota has emerged as a key modulator of host immune responses, and growing evidence suggests it plays a role in shaping vaccine-induced immunity. While immunization remains vital for preventing infectious diseases, inter-individual variability in vaccine responses poses a persistent challenge. Traditional factors such as age, sex, genetics, and immune status do not fully account for this variability. Recent studies highlight the gut microbiome as a potential contributor. This review examines current evidence linking the gut microbiota to vaccine responses, with a focus on vaccines against SARS-CoV-2, hepatitis B virus, and influenza. Human studies show associations between microbial composition, particularly taxa like Bifidobacterium adolescentis, and immunogenicity. Microbial metabolites, such as short-chain fatty acids and bile acids, influence T-cell differentiation, antibody production, and cytokine responses. Factors that alter microbiota composition, including antibiotics, diet, and prebiotic or probiotic supplementation, can impact vaccine responses, highlighting a dynamic gut-immune relationship. Experimental models further support these observations, showing diminished responses in germ-free or antibiotic-treated animals and enhanced responses following microbial-based interventions. These findings also suggest the gut microbiota may be harnessed to improve vaccine efficacy. Future research should explore the potential for microbiota-targeted strategies to optimize vaccine efficacy, particularly in immunocompromised populations.
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Journal articleCassir N, Ghani R, Biehl LM, et al., 2025,
Nonantimicrobial therapies for recurrent urinary tract infection in women: is there a place for faecal microbiota transfer?
, Clinical Microbiology and Infection, Vol: 31, Pages: 1985-1992, ISSN: 1198-743X -
Journal articleMullish BH, Javed A, Ghani R, et al., 2025,
Operational considerations for the running of an NHS faecal microbiota transplant service
, Journal of Hospital Infection, Vol: 164, Pages: 105-110, ISSN: 0195-6701 -
Journal articleMichael DR, John DA, Coates N, et al., 2025,
The impact of three distinct probiotic supplements on the gut microbiota and its metabolites in healthy adults.
, Benef Microbes, Vol: 17, Pages: 221-234The effects of probiotics on the gut microbiota and microbial metabolites in healthy individuals are not well understood. Faecal and serum samples were collected at the start and end of a 3-month, double-blind, placebo-controlled, randomised study with three different probiotic formulations in free-living, healthy adults. The composition of the faecal microbiota and levels of faecal and/or serum short-chain fatty acids (SCFA) and bile acids (BA) were measured and the probiotic formulations were found to impart differing effects including shifts in the composition and structure of the faecal microbiota, enhanced levels of circulating short chain fatty acids such as butyrate and propionate, and elevated levels of sulphated bile acids in faeces. This was in contrast to the outcomes for the placebo population where very little change occurred over the study. These findings demonstrate that probiotic supplementation elicits formulation specific effects and that there are potential benefits for healthy individuals.
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Journal articleMullish BH, Ianiro G, 2025,
Preface to special edition: Microbiome, inflammation and cancer
, Best Practice & Research Clinical Gastroenterology, Vol: 77, Pages: 101952-101952, ISSN: 1521-6918 -
Journal articleKing OG, Yip AYG, Horrocks V, et al., 2025,
Vancomycin-resistant enterococci utilise antibiotic-enriched nutrients for intestinal colonisation
, Nature Communications, Vol: 16<jats:title>Abstract</jats:title> <jats:p> Antibiotic treatment significantly disrupts the gut microbiome and promotes vancomycin-resistant enterococci (VRE) intestinal colonisation. These disruptions cause the intestine to act as a reservoir for VRE that seed difficult-to-treat infections. Here we show that antibiotics that promote VRE intestinal colonisation increase the concentration of a wide range of nutrients and decrease the concentration of a wide range of microbial metabolites. We show significant but incomplete suppression of VRE growth by individual short chain fatty acids that were decreased in antibiotic-treated faecal microbiomes. However, mixtures of short chain fatty acids provide complete or near complete suppression of VRE growth. We show that VRE use most nutrients increased in antibiotic-treated faecal microbiomes as carbon or nitrogen sources to support their growth, where <jats:italic>Enterococcus faecium</jats:italic> and <jats:italic>Enterococcus faecalis</jats:italic> have some common and some distinct preferences for the use of these specific nutrients. Finally, we show that <jats:italic>E. faecium</jats:italic> and <jats:italic>E. faecalis</jats:italic> occupy overlapping but distinct nutrient-defined intestinal niches that promote high growth when cultured with each other and when cultured with carbapenem-resistant <jats:italic>Enterobacteriaceae</jats:italic> . Our results demonstrate that VRE occupy distinct intestinal niches in the antibiotic-treated intestine, defined by their abilities to utilise specific enriched nutrients and their abilities to grow with reduced concentrations of inhibitory microbial metabolites. <
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Journal articleUmamahesan C, Pilcicka A, Yick J, et al., 2025,
Interplay of constipation, intestinal barrier dysfunction and fungal exposome in aetiopathogenesis of Parkinson’s disease: hypothesis with supportive data
, Biochemical Journal, Vol: 482, Pages: 807-821, ISSN: 0264-6021<jats:p>Constipation is a forerunner to Parkinson’s disease (PD) diagnosis, worsening thereafter. We explore the relationship of intestinal barrier dysfunction to constipation and whether intestinal fungal load is an aggravating factor. Fungal load was quantified by real-time PCR, using ITS1F-ITS2 primer set, on microbial DNA extract from stool in 68 participants with PD, 102 without. Fungal load was 60% higher per decade after age 60 years, with no PD status interaction with age. After age adjustment, it was associated inversely with dietary renal acid load. It was unrelated to the presence of constipation or barrier dysfunction. Neither consumption of antimicrobials nor of other targeted exogenous substances was associated. Enzyme-linked immunosorbent assays measured barrier dysfunction markers, faecal alpha-1 antitrypsin (AAT), zonulin and serum intestinal fatty acid-binding protein (I-FABP). Barrier dysfunction was associated with constipation and slower radiographic colonic transit. Functional constipation was 28% more frequent with a doubling of AAT concentration. More colonic-transit test markers were retained in the transverse colon, the higher the AAT and zonulin concentrations, anatomically spotlighting abnormality for the entire colon. In contrast, the concentration of the small intestinal barrier marker I-FABP was associated with looser stool consistency, which is consistent with secondary microbial overgrowth. By showing a relationship of intestinal barrier dysfunction to constipation, this study supports the hypothesis that dysfunction may be consequential. Dysfunction may be a necessary, but not sufficient, precursor to PD, in allowing inflammaging. Since ageing is the clearest risk for PD, a gut pathogen escalating in abundance from the sixth decade, integral to fungal load, and whose reproduction and virulence is favoured by alkalinity, tallies.</jats:p>
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Journal articleQuraishi MN, Cheesbrough J, Rimmer P, et al., 2025,
Open Label Vancomycin in Primary Sclerosing Cholangitis-Inflammatory Bowel Disease: Improved Colonic Disease Activity and Associations With Changes in Host–Microbiome–Metabolomic Signatures
, Journal of Crohn's and Colitis, Vol: 19, ISSN: 1873-9946<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Background</jats:title> <jats:p>We conducted a single-arm interventional study, to explore mucosal changes associated with clinical remission under oral vancomycin (OV) treatment, in primary sclerosing cholangitis-associated inflammatory bowel disease (PSC-IBD); NCT05376228.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>Fifteen patients with PSC and active colitis (median fecal calprotectin 459 µg/g; median total Mayo score 5) were treated with OV (125 mg QID) for 4 weeks and followed-up for a further 4 weeks of treatment withdrawal (8 weeks, end-of-study). Colonic biopsies were obtained at baseline and Week 4. Clinical assessments, and serum and stool samples (metagenomics, metatranscriptomics, and metabolomics) were collected at Weeks 0, 2, 4, and 8. The primary efficacy outcome measure was the induction of clinical remission.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Oral vancomycin resulted in clinical remission in 12/15 patients and significant reductions in fecal calprotectin. Oral vancomycin was associated with reduced abundances of Lachnospiraceae, genera Blautia and Bacteroides; and enrichment of Enterobacteriaceae, and genera Veillonella, Akkermansia, and Escherichia. Oral vancomycin treatment was associated with the downregulation of multiple metatranscriptomic pathways (including short-chain fatty acid [SCFA] metabolism and bile acid [BA] biotransformation), along with host genes and multiple pathways involved in inflammatory responses and antimicrobial defence; and an upregulation of genes associated with extracellular matrix repair. Oral vancomycin use r
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Journal articlePorcari S, Mullish BH, Asnicar F, et al., 2025,
International consensus statement on microbiome testing in clinical practice
, The Lancet Gastroenterology & Hepatology, Vol: 10, Pages: 154-167, ISSN: 2468-1253 -
Journal articleAl-Shakhshir S, Quraishi MN, Mullish B, et al., 2025,
FAecal micRobiota transplantation in primary sclerosinG chOlangitis (FARGO): study protocol for a randomised, multicentre, phase IIa, placebo-controlled trial
, BMJ Open, Vol: 15, Pages: e095392-e095392, ISSN: 2044-6055<jats:sec> <jats:title>Introduction</jats:title> <jats:p>Primary sclerosing cholangitis (PSC) is the classical hepatobiliary manifestation of inflammatory bowel disease (IBD). The strong association between gut and liver inflammation has driven several pathogenic hypotheses to which the intestinal microbiome is proposed to contribute. Pilot studies of faecal microbiota transplantation (FMT) in PSC and IBD are demonstrated to be safe and associated with increased gut bacterial diversity. However, the longevity of such changes and the impact on markers of disease activity and disease progression have not been studied. The aim of this clinical trial is to determine the effects of repeated FMT as a treatment for PSC-IBD.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods and analysis</jats:title> <jats:p>FAecal micRobiota transplantation in primary sclerosinG chOlangitis (FARGO) is a phase IIa randomised placebo-controlled trial to assess the efficacy and safety of repeated colonic administration of FMT in patients with non-cirrhotic PSC-IBD. Fifty-eight patients will be recruited from six sites across England and randomised in a 1:1 ratio between active FMT or FMT placebo arms. FMT will be manufactured by the University of Birmingham Microbiome Treatment Centre, using stool collected from rigorously screened healthy donors. A total of 8 weekly treatments will be delivered; the first through colonoscopic administration (week 1) and the remaining seven via once-weekly enema (up to week 8). Participants will then be followed on a 12-weekly basis until week 48 from the first treatment visit. The primary efficacy outcome will be to determine the effect of FMT on serum alkaline phosphatase values over time (end of study at 48 weeks). Key secondary outcomes will be to evaluate the impact of FMT on oth
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