ArticleGut and liver2010
The role of bacteria in the pathogenesis of inflammatory bowel disease.
Article in Gut and liver, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- The diagnostic value of polymerase chain reaction forSaudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationPooled it
- Trial
- A Review on Functional Foods Regulate the Gut Microbiota and Mast Cell Function in Inflammatory Bowel Disease (IBD).Probiotics and antimicrobial proteins · 2026Review
- Canonical pathways and selective mechanisms of autophagy in inflammatory bowel disease.Advanced biotechnology · 2026Review
- Bidirectional Interplay Between IBD Therapies and the Gut Microbiota: A Pharmacomicrobiomic Approach to Personalized Treatment.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025Review
- Cystic fibrosis and inflammatory bowel disease: parallels in gut physiology and microbiota.Journal of bacteriology · 2025Review
- Akkermansia muciniphila improve cognitive dysfunction by regulating BDNF and serotonin pathway in gut-liver-brain axis.Microbiome · 2024Article
- Oral Administration ofMicroorganisms · 2023Article
- Offense and Defense in Granulomatous Inflammation Disease.Frontiers in cellular and infection microbiology · 2022Review
- Cellular Immune Signal Exchange From Ischemic Stroke to Intestinal Lesions Through Brain-Gut Axis.Frontiers in immunology · 2022Review
- Nanotechnology as a Novel Approach in Combating Microbes Providing an Alternative to Antibiotics.Antibiotics (Basel, Switzerland) · 2021Review
- Microbiota-Immune Interactions in Ulcerative Colitis and Colitis Associated Cancer and Emerging Microbiota-Based Therapies.International journal of molecular sciences · 2021Review
- Comparative Pathogenomics ofInfection and immunity · 2021Article
- F. prausnitzii and its supernatant increase SCFAs-producing bacteria to restore gut dysbiosis in TNBS-induced colitis.AMB Express · 2021Article
- Alteration of Gut Microbiota in Inflammatory Bowel Disease (IBD): Cause or Consequence? IBD Treatment Targeting the Gut Microbiome.Pathogens (Basel, Switzerland) · 2019Review
- Molecular profiling of mucosal tissue associated microbiota in patients manifesting acute exacerbations and remission stage of ulcerative colitis.World journal of microbiology & biotechnology · 2018Article
- PersistentFrontiers in immunology · 2018Article
- Uridine Ameliorates Dextran Sulfate Sodium (DSS)-Induced Colitis in Mice.Scientific reports · 2017Article
- PROBIOTICS - A PROBABLE THERAPEUTIC AGENT FOR SPONDYLOARTHROPATHY.International journal of probiotics & prebiotics · 2017Article
- Bacteriophages in the gastrointestinal tract and their implications.Gut pathogens · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Crohn's disease (CD) and ulcerative colitis (UC) have features that suggest bacterial involvement, and all genetic models of inflammatory bowel disease (IBD) require the presence of commensal bacteria. CD is associated with innate immune response genes such as NOD2/CARD15 and the autophagy genes ATG16L1 and IRGM. However, IBD responds to immunosuppression, suggesting that any bacteria involved are not acting as conventional pathogens. Molecular techniques are rapidly advancing our knowledge of the gut microbiota. In CD there is reduced diversity, and notably a reduction in the probiotic Faecalibacterium prausnitzii, the presence of which in the terminal ileum is associated with a reduced risk of recurrence following surgery. There is also a consistent increase in mucosa-associated Escherichia coli with an "adherent and invasive" phenotype, which allows them to replicate inside macrophages and induce granulomas. Speculation that CD could be caused by the Mycobacterium avium subspecies paratuberculosis (MAP) continues. The response to antitumor necrosis factor treatments suggests that, if relevant at all, MAP is not acting as a conventional pathogen. However, there is increased colonization by MAP in CD, and there is evidence that it could have an indirect effect mediated by the suppression of macrophage function. UC relapse is frequently associated with infection by pathogens, but there is less evidence for involvement of a specific bacterial species. Poor barrier integrity followed by an inflammatory reaction to bacterial components, with chronicity maintained by an autoimmune process, seems a plausible pathogenic model. Bacterial theories of pathogenesis are now becoming testable by targeted therapeutic interventions.
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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.