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Fibrogenesis in chronic murine colitis is independent of innate lymphoid cells

Authors
  • Creyns, Brecht; 105567;
  • Cremer, Jonathan; 56137;
  • De Hertogh, Gert; 41158;
  • Boon, Louis;
  • Ferrante, Marc; 45367;
  • Vermeire, Severine; 3938;
  • Van Assche, Gert;
  • Ceuppens, Jan L; 14358;
  • Breynaert, Christine; 69617;
Publication Date
Jun 21, 2020
Source
Lirias
Keywords
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Unknown
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Abstract

INTRODUCTION: Insight in the pathogenesis of intestinal fibrosis is an unmet medical need in inflammatory bowel diseases. Studies in murine models and human organ fibrosis point to a potential role of innate lymphoid cells (ILC) in chronic intestinal inflammation and fibrosis. MATERIALS AND METHODS: Dextran sodium sulfate (DSS) in drinking water was used to induce chronic colitis and remodeling in C57Bl/6 wild type (WT), RAG-deficient, RAG-/- common γ chain deficient and anti-CD90.2 monoclonal antibody treated RAG-/- mice. Inflammation was scored by macroscopic and histological examination and fibrosis was evaluated by hydroxyproline quantification and histology. RESULTS: In RAG-/- mice (which have a normal ILC population but no adaptive immunity), chronic intestinal inflammation and fibrosis developed similarly as in WT mice, with a relative increase in ILC2 during repeated DSS exposure. Chronic colitis could also be induced in the absence of ILC (RAG-/- γc-/- or anti-CD90.2 treated RAG-/- mice) with no attenuation of fibrosis. Importantly, clinical recovery based on weight gain after stopping DSS exposure was impaired in ILC-deficient or ILC-depleted mice. CONCLUSION: These data argue against a profibrotic effect of ILC in chronic colitis, but rather suggest that ILC have a protective and recovery-enhancing effect after repeated intestinal injury. / status: published

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