title: Genetic deletion of dectin-1 does not affect the course of murine experimental colitis.
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.
authors.affiliation: Tytgat Institute for Liver and Intestinal Research, Academic Medical Center, University of Amsterdam, AMC, Amsterdam, The Netherlands. s.e.heinsbroek@amc.uva.nl
authors.forename: Sigrid Em
authors.initials: SE
authors.lastname: Heinsbroek
authors.forename: Anneke
authors.initials: A
authors.lastname: Oei
authors.forename: Joris J T H
authors.initials: JJ
authors.lastname: Roelofs
authors.forename: Shobhit
authors.initials: S
authors.lastname: Dhawan
authors.forename: Anje
authors.initials: A
authors.lastname: te Velde
authors.forename: Siamon
authors.initials: S
authors.lastname: Gordon
authors.forename: Wouter J
authors.initials: WJ
authors.lastname: de Jonge
mesh_terms: D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000235:genetics* / Q000276:immunology* / Q000382:microbiology; D016264:Dextran Sulfate; D005243:Feces / Q000382:microbiology; D044923:Helicobacter hepaticus; D016753:Interleukin-10 / Q000378:metabolism; D007420:Intestine, Large / Q000382:microbiology; D037181:Lectins, C-Type / Q000235:genetics* / Q000276:immunology*; D008070:Lipopolysaccharides / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D054892:Metagenome; D051379:Mice; D008810:Mice, Inbred C57BL; D012248:Rhodotorula / Q000276:immunology; D013682:Teichoic Acids / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015054:Zymosan / Q000276:immunology; D000099181:Dectin-1
chemical_list: D016264:Dextran Sulfate; D016753:Interleukin-10; D037181:Lectins, C-Type; D008070:Lipopolysaccharides; D013682:Teichoic Acids; D014409:Tumor Necrosis Factor-alpha; D015054:Zymosan; D000099181:Dectin-1; C009900:lipoteichoic acid