NOD2-dependent licensing of the microbiota predispose to transmissible inflammation and tumorigenesis in the colon.

ABSTRACT: Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as CrohnM-bM-^@M-^Ys disease and colorectal cancer. Here, we show that dysbiosis coupled to Nod2 or Rip2 deficiency suffices to cause an increased risk for intestinal inflammation and colitis-associated carcinogenesis in mice. Aggravated epithelial lesions and dysplasia upon chemical-induced injury associated with loss of Nod2 or Rip2 can be prevented by antibiotics or anti-IL6R treatment. Nod2-mediated risk for intestinal inflammation and colitis-associated tumorigenesis is communicable through maternally-transmitted microbiota even to wild-type hosts. Disease progression was identified to drive complex NOD2-dependent changes of the colonic

ORGANISM(S): Mus musculus

SUBMITTER: David Hot 

PROVIDER: E-GEOD-32421 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress