Selective deletion of MyD88 signaling in α-SMA positive cells ameliorates experimental intestinal fibrosis via post-transcriptional regulation
Open accessAbstract
Intestinal fibrosis leading to strictures remains a significant clinical problem in inflammatory bowel diseases (IBD). The role of bacterial components in activating intestinal mesenchymal cells and driving fibrogenesis is largely unexplored. Tamoxifen-inducible α-SMA promoter Cre mice crossed with floxed MyD88 mice were subjected to chronic dextran sodium sulfate colitis. MyD88 was deleted prior to or after induction of colitis. Human intestinal myofibroblasts (HIMF) were exposed to various bacterial components and assessed for fibronectin (FN) and collagen I (Col1) production. RNA sequencing was performed. Post-transcriptional regulation was assessed by polysome profiling assay. Selective deletion of MyD88 in α-SMA-positive cells prior to, but not after induction of, experimental colitis decreased the degree of intestinal fibrosis. HIMF selectively responded to flagellin with enhanced FN or Col1 protein production in a MyD88-dependent manner. RNA sequencing suggested minimal transcriptional changes induced by flagellin in HIMF. Polysome profiling revealed higher proportions of FN and Col1 mRNA in the actively translated fractions of flagellin exposed HIMF, which was mediated by eIF2 alpha and 4EBP1. In conclusion, selectivity of flagellin-induced ECM secretion in HIMF is post-transcriptionally regulated. The results may represent a novel and targetable link between the gut microbiota and intestinal fibrogenesis.
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- Authors
- Zhao, S., Dejanovic, D., Yao, P., Bhilocha, S., Sadler, T., Schirbel, A., West, G., Doyon, G., Lopez, R., Mao, R., Kurada, S., El Ouali, S., Grassl, G., Fox, P. L., Cruise, M., Worthley, D. L., de la Motte, C., Fiocchi, C., & Rieder, F.
- Affiliations
- Cleveland Clinic (US)
- Christian-Albrechts-Universität zu Kiel (DE)
- South Australian Health and Medical Research Institute (AU)
- Corresponding author
- Rieder, Florian
- ORCID
- Venue
- Mucosal Immunology
- Publisher
- Elsevier BV
- Published
- 2020-07
- Volume
- 13
- Issue
- 4
- Pages
- 665-678
- ISSN
- 1933-0219 (ISSN-L)
- PMC
- PMC7316631
- OpenAlex
- W3004467012
- Cited by
- 59
- References
- 70
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 15 · 2023: 3 · 2022: 7 · 2021: 14 · 2020: 4
- FWCI
- 4.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Mucosal Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Crohn's and Colitis Foundation of America
- University of Chicago
- Cleveland Clinic
- Crohn's and Colitis Foundation (569125)
- IFM Therapeutics
- Deutsche Forschungsgemeinschaft
- National Institutes of Health (UL1TR000439, UL1TR002548, P30DK097948 Pilot)
- National Heart, Lung, and Blood Institute (R01HL147954, R01HL132899)
- National Institute of Diabetes and Digestive and Kidney Diseases (K08DK110415, R01DK050984, R01DK069854, P30DK097948, T32DK083251)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Epidemiology › Microscopic Colitis
- Keywords
- MyD88 signaling, intestinal fibrosis, intestinal stenosis, inflammatory bowel disease, DSS-induced colitis, intestinal myofibroblasts, flagellin, post-transcriptional regulation, polysome profiling, eIF2α, 4E-BP1, extracellular matrix secretion, fibronectin, type I collagen, gut microbiota, mesenchymal cells
- MeSH terms
- Actins, Animals, Cells, Cultured, Disease Susceptibility, Extracellular Matrix, Fibroblasts, Fibrosis, Fluorescent Antibody Technique, Gene Expression Regulation, Humans, Immunohistochemistry, Intestinal Mucosa, RNA Processing, Post-Transcriptional, Signal Transduction, Biomarkers, Gene Expression Profiling, Mice, Myeloid Differentiation Factor 88
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