Dysbiosis in inflammatory bowel disease


Abundant data have incriminated intestinal bacteria in the initiation and amplification stages of inflammatory bowel diseases (IBD).12The role of the NOD2/CARD15 Crohn’s disease (CD) susceptibility gene in bacterial peptidoglycan recognition strengthens the links between enteric bacteria and mucosal inflammation.3–5 Despite these advances, the precise role of intestinal bacteria remains elusive. Nonmutually exclusive theories have included: an unidentified persistent pathogen; an abnormally permeable mucosal barrier leading to excessive bacterial translocation; an immune system abnormality of effector cell activation or insufficient regulatory cell activity in response to intestinal bacteria67; or a breakdown in the balance between putative species of ‘‘protective’’ versus ‘‘harmful’’ intestinal bacteria—this concept has been termed ‘‘dysbiosis’’.89Here we will focus on arguments to support this concept.

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