1. Introduction
Observations of inflammatory bowel disease (IBD) have led to the
theory that the pathogenesis of IBD is the result of an aberrant
immune response to normal commensal bacteria in genetically
susceptible individuals (Khor et al., 2011; Xavier and Podolsky,
2005). In humans, the intestinal bacterial community (microbiota)
that inhabits in the gut appears to be an important source of antigens,
which drive the chronic immunologic processes that are hallmarks of
both Crohn's disease (CD) and ulcerative colitis (UC). Although
several bacterial and viral pathogens have been suggested as causes of
IBD, none has gained general acceptance. Current views assert that
the pathology of IBD is a result of members in gut microbiota. These
commensal bacteria are believed to be the source of antigens to which
the dysfunctional immune system reacts. The distal gut of humans is
one of the most densely populated microbial ecosystems on Earth.
The endogenous gastrointestinal microbiota fulfills a fundamental