ArticleBMC medicine2025
Faecalibacterium prausnitzii enhances intestinal IgA response by host-microbe derived inecalcitol in colitis.
Article in BMC medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- Faecalibacterium prausnitzii EXL01 for the Maintenance of Steroid-induced Clinical Response or Remission in Patients with Crohn's Disease: a first in human trial.Nature communications · 2026Trial
- Short-chain fatty acid-producing commensals: Key modulators of AD neuroinflammation via the microbiota-gut-brain axis.Current research in microbial sciences · 2026Review
- Faecalibacterium prausnitzii: Mechanistic Insights and Therapeutic Potential in Host-Microbe Crosstalk.Probiotics and antimicrobial proteins · 2026Review
- Article
- Microbial engraftment and immune regulation during fecal microbiota transplantation and immune checkpoint inhibitor therapy.Nature communications · 2026Review
- Microbiota-gut-brain axis and neuroendocrine pathways underlie divergent mechanisms of intermittent and continuous theta-burst stimulation in autism spectrum disorder.Cellular and molecular life sciences : CMLS · 2026Article
- Raspberry aqueous extract ameliorates MAFLD in mice by regulating gut microbiota and purine metabolism.Frontiers in nutrition · 2026Article
- Fecal microbiota transplantation in ulcerative colitis: mucosal immune mechanisms and precision microbiota therapy.Frontiers in immunology · 2026Review
- Acupuncture modulates the microbiota-gut-brain axis to treat irritable bowel syndrome: a mechanistic exploration.Frontiers in neuroscience · 2026Review
- Secondary Bile Acids Modified by Odoribacter Splanchnicus Alleviate Colitis by Suppressing Neutrophil Extracellular Trap Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundFaecalibacterium prausnitzii plays a crucial role in ulcerative colitis (UC) remission, but its action mechanism is unknown. Here, we aimed to explore the potential mechanisms focusing on the interaction of F. prausnitzii with host immune response and its potential modulation on gut microbiome.
methodsRNA-seq analysis together with 16S rRNA sequencing and metabolomics were performed in a dextran sodium sulfate (DSS)-induced colitis mouse model followed by F. prausnitzii gavage. To present evidence of sIgA involved in the anti-inflammatory effects of F. prausnitzii, we further applied immunoglobulin A (IgA) knockout mice and secretory IgA (sIgA) depletion mouse models using polymeric immunoglobulin receptor (pIgR) neutralizing antibody. Colonic immune cells were characterized by flow cytometry. The fecal relative abundance of F. prausnitzii, inecalcitol, and colonic IgA expression were assessed in UC patients.
resultsF. prausnitzii markedly ameliorated colitis by alleviating intestinal inflammation and barrier dysfunction, with significantly decreased abundance of pro-inflammatory taxa (Enterococcus, Desulfovibrio, Escherichia-Shigella, and Enterorhabdus) and increased abundance of Lachnospiraceae NK4A136_group. Functions related to intestinal immune network for IgA production pathway were up-regulated shown by transcriptomics and KEGG pathway analysis. Increased expression of IgA production associated genes including MHCII-related genes, Aicda, and Tnfrsfl3c were verified, accompanied by up-regulated colonic IgA and pIgR. The IgA knockout mice and sIgA depletion model weakened the anti-inflammation and microbiota-modulation effects of F. prausnitzii, which was further proved by fecal microbiota transplantation (FMT). The shift profile of fecal metabolites after F. prausnitzii supplement was characterized by increased production of inecalcitol, which may account for the enhanced IgA response. In a cohort of UC patients, the relative abundance of F. prausnitzii was decreased and positively correlated with colonic IgA expression and negatively correlated with disease severity.
conclusionsF. prausnitzii effectively alleviated colonic inflammation and modulated dysbiosis via enhancing colonic IgA response, thus showing promise as a UC treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.