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Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
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Campylobacter concisus and inflammatory bowel disease.
Li Zhang1, Hoyul Lee1, Michael C Grimm1
1Li Zhang, Hoyul Lee, School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia.
World Journal of Gastroenterology
|February 28, 2014
Summary
Campylobacter concisus (C. concisus) may trigger inflammatory bowel disease (IBD) by producing a toxin that increases intestinal permeability. This oral bacterium
Area of Science:
- Microbiology
- Gastroenterology
- Immunology
Background:
- Campylobacter concisus (C. concisus) is increasingly associated with inflammatory bowel disease (IBD).
- The mechanism by which oral C. concisus contributes to gut inflammation remains unclear.
- Increased intestinal permeability is a hallmark of IBD.
Purpose of the Study:
- To investigate the role of C. concisus in IBD pathogenesis.
- To explore the potential mechanism involving the zonula occludens toxin (zot).
Main Methods:
- Review of existing evidence on C. concisus, zot, and IBD.
- Comparative analysis of C. concisus Zot with Vibrio cholerae Zot and human zonulin.
- Assessment of the impact on intestinal tight junctions and permeability.
Main Results:
- Some C. concisus strains possess the zonula occludens toxin (zot) gene acquired from a prophage.
- C. concisus Zot shares functional motifs with known intestinal permeability-increasing proteins.
- These toxins affect tight junctions, potentially increasing intestinal permeability.
Conclusions:
- C. concisus Zot may induce intestinal barrier dysfunction.
- This barrier defect is a proposed mechanism linking zot-positive C. concisus to IBD onset and relapse.
- Further research into C. concisus as an IBD trigger is warranted.
Keywords:
Campylobacter concisusInflammatory bowel diseaseIntestinal permeabilityTight junctionsZonula occludens toxinMore Related Videos
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