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NLRP6 inflammasome regulates colonic microbial ecology and risk for colitis.

Inflammasomes are multiprotein complexes that function as sensors of endogenous or exogenous damage-associated molecular patterns. Here, we show that deficiency of NLRP6 in mouse colonic epithelial cells results in reduced IL-18 levels and altered fecal microbiota characterized by expanded representation of the bacterial phyla Bacteroidetes (Prevotellaceae) and TM7. NLRP6 inflammasome-deficient mice were characterized by spontaneous intestinal hyperplasia, inflammatory cell recruitment, and exacerbation of chemical colitis induced by exposure to dextran sodium sulfate (DSS). Cross-fostering and cohousing experiments revealed that the colitogenic activity of this microbiota is transferable to neonatal or adult wild-type mice, leading to exacerbation of DSS colitis via induction of the cytokine, CCL5. Antibiotic treatment and electron microscopy studies further supported the role of Prevotellaceae as a key representative of this microbiota-associated phenotype. Altogether, perturbations in this inflammasome pathway, including NLRP6, ASC, caspase-1, and IL-18, may constitute a predisposing or initiating event in some cases of human IBD.

Pubmed ID: 21565393


  • Elinav E
  • Strowig T
  • Kau AL
  • Henao-Mejia J
  • Thaiss CA
  • Booth CJ
  • Peaper DR
  • Bertin J
  • Eisenbarth SC
  • Gordon JI
  • Flavell RA



Publication Data

May 27, 2011

Associated Grants

  • Agency: Howard Hughes Medical Institute, Id:
  • Agency: Howard Hughes Medical Institute, Id:

Mesh Terms

  • Animals
  • Bacteria
  • Bacteroidetes
  • Chemokine CCL5
  • Colitis
  • Colon
  • Dextran Sulfate
  • Disease Susceptibility
  • Inflammasomes
  • Interleukin-18
  • Mice
  • Mice, 129 Strain
  • Mice, Inbred C57BL
  • Receptors, Cell Surface