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

BMC Gastroenterol. 2012 Apr 16:12:33. doi: 10.1186/1471-230X-12-33.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Colitis / chemically induced
  • Colitis / genetics*
  • Colitis / immunology*
  • Colitis / microbiology
  • Dextran Sulfate
  • Feces / microbiology
  • Helicobacter hepaticus
  • Interleukin-10 / metabolism
  • Intestine, Large / microbiology
  • Lectins, C-Type / genetics*
  • Lectins, C-Type / immunology*
  • Lipopolysaccharides / immunology
  • Macrophages / immunology*
  • Metagenome
  • Mice
  • Mice, Inbred C57BL
  • Rhodotorula / immunology
  • Teichoic Acids / immunology
  • Tumor Necrosis Factor-alpha / metabolism
  • Zymosan / immunology

Substances

  • Lectins, C-Type
  • Lipopolysaccharides
  • Teichoic Acids
  • Tumor Necrosis Factor-alpha
  • dectin 1
  • Interleukin-10
  • lipoteichoic acid
  • Zymosan
  • Dextran Sulfate