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Updated: May 23, 2026
Murine Distal Colostomy, A Novel Model of Diversion Colitis in C57BL/6 Mice
Published on: July 12, 2018
Genetic deletion of dectin-1 does not affect the course of murine experimental colitis
Sigrid Em Heinsbroek1, Anneke Oei, Joris J T H Roelofs
1Tytgat Institute for Liver and Intestinal Research, Academic Medical Center, University of Amsterdam, AMC, Amsterdam, The Netherlands. s.e.heinsbroek@amc.uva.nl
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.
