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Inflammation-independent TL1A-mediated intestinal fibrosis is dependent on the gut microbiome
Open accessAbstract
Tumor necrosis factor-like cytokine 1A (TL1A, TNFSF15) is implicated in inflammatory bowel disease (IBD), modulating the location and severity of intestinal inflammation and fibrosis. TL1A expression is increased in inflamed gut mucosa and associated with fibrostenosing Crohn's disease. Tl1a-overexpression in mice lead to spontaneous ileitis, and exacerbated induced proximal colitis and fibrosis. IBD is associated with shifts in the gut microbiome, but the effect of differing microbial populations and their interaction with TL1A on fibrosis has not been investigated. We demonstrate that the pro-fibrotic and inflammatory phenotype resulting from Tl1a-overexpression is abrogated in the absence of resident microbiota. To evaluate if this is due to the absence of a unique bacterial population, as opposed to any bacteria per se, we gavaged germ-free (GF) wild-type and Tl1a-transgenic (Tl1a-Tg) mice with stool from specific pathogen free (SPF) mice and a healthy human donor (Hu). Reconstitution with SPF, but not Hu microbiota, resulted in increased intestinal collagen deposition and fibroblast activation in Tl1a-Tg mice. Notably, there was reduced fibroblast migration and activation under GF conditions compared to native conditions. We then identified several candidate organisms that correlated directly with increased fibrosis in reconstituted mice and showed that these organisms directly impact fibroblast function in vitro. Thus, Tl1a-mediated intestinal fibrosis and fibroblast activation are dependent on specific microbial populations.
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“Increased liver ECM deposition was observed in germ free mice compared to conventionally housed mice166, which was also observed in MyD88/TRIF deficient mice.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [166]
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Anti-fibrotic Drugs for Crohn’s Disease: Ready for Prime Time?
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TNFSF15 variant predicts disease progression in Chinese patients with Crohn’s disease
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Metadata
- Authors
- Jacob, N., Jacobs, J. P., Kumagai, K., Ha, C. W. Y., Kanazawa, Y., Lagishetty, V., Altmayer, K., Hamill, A. M., Von Arx, A., Sartor, R. B., Devkota, S., Braun, J., Michelsen, K. S., Targan, S. R., & Shih, D. Q.
- Affiliations
- Cedars-Sinai Medical Center (US)
- University of California, Los Angeles (US)
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Jacob, Noam
- Shih, David Q.
- ORCID
- Venue
- Mucosal Immunology
- Publisher
- Elsevier BV
- Published
- 2018-09
- Volume
- 11
- Issue
- 5
- Pages
- 1466-1476
- ISSN
- 1933-0219 (ISSN-L)
- PMC
- PMC6162160
- OpenAlex
- W2863875449
- Cited by
- 102
- References
- 51
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 18 · 2023: 10 · 2022: 12 · 2021: 21 · 2020: 12 · 2019: 5 · 2018: 2
- FWCI
- 6.12
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Mucosal Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Crohn's and Colitis Foundation
- National Institutes of Health (NIH T32, NIH-R01, DK034987, DK056328, T32DK07180—40, P40OD010995)
- Inflammatory Bowel and Immunobiology Research Institute
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK046763, K08DK093578, P01DK094779, P30DK041301, R01DK056328, L30 DK110927, T32DK007180, P30DK034987)
- Topics
- Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Microscopic Colitis
- Keywords
- TL1A, TNFSF15, intestinal fibrosis, gut microbiota, inflammatory bowel disease, Crohn's disease, fibroblast activation, fibroblast migration, germ-free mice, transgenic mice, collagen deposition
- MeSH terms
- Gastrointestinal Microbiome, Animals, Colitis, Collagen, Crohn Disease, Fibroblasts, Fibrosis, Humans, Ileitis, Inflammation, Intestinal Mucosa, Intestines, Mice, Inbred C57BL, Mice, Transgenic, Inflammatory Bowel Diseases, Mice, Tumor Necrosis Factor Ligand Superfamily Member 15
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