Genetic deletion of dectin-1 does not affect the course of murine experimental colitis

Sigrid E.M. Heinsbroek*, Anneke Oei, Joris J.T.H. Roelofs, Shobhit Dhawan, Anje te Velde, Siamon Gordon, Wouter J. de Jonge

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

20 Scopus citations

Abstract

Background: It is believed that inflammatory bowel diseases (IBD) result from an imbalance in the intestinal immune response towards the luminal microbiome. Dectin-1 is a widely expressed pattern recognition receptor that recognizes fungi and upon recognition it mediates cytokine responses and skewing of the adaptive immune system. Hence, dectin-1 may be involved in the pathogenesis of IBD.Methods: We assessed the responses of dectin-1 deficient macrophages to the intestinal microbiota and determined the course of acute DSS and chronic Helicobacter hepaticus induced colitis in dectin-1 deficient mice.Results: We show that the mouse intestinal microbiota contains fungi and the cytokine responses towards this microbiota were significantly reduced in dectin-1 deficient macrophages. However, in two different colitis models no significant differences in the course of inflammation were found in dectin-1 deficient mice compared to wild type mice.Conclusions: Together our data suggest that, although at the immune cell level there is a difference in response towards the intestinal flora in dectin-1 deficient macrophages, during intestinal inflammation this response seems to be redundant since dectin-1 deficiency in mice does not affect intestinal inflammation in experimental colitis.

Original languageEnglish
Article number33
JournalBMC Gastroenterology
Volume12
DOIs
StatePublished - 16 04 2012
Externally publishedYes

Keywords

  • Colitis
  • Dectin-1
  • Fungi
  • Innate immunity
  • Intestine
  • Macrophages

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