The two major inflammatory bowel diseases (IBD), Crohn’s disease (CD), and ulcerative colitis (UC) are idiopathic relapsing disorders characterized by chronic inflammation of the gastrointestinal tract. It is increasingly evident that the commensal intestinal microbiota plays a role in the pathogenesis of IBD, as multiple lines of evidence, both from rodent and human studies, support microbial involvement in the etiology of these diseases. In general, it is thought that IBD are driven by an irregular immune response to the commensal microbiota in genetically susceptible individuals. A leading hypothesis, concerning the nature of the role that bacteria play in the pathogenesis of IBD, suggests that the disease state is promoted by dysbiosis, a shift in the balance of healthy microbiota in favor of pro-inflammatory microbial species. Numerous studies have described a reduction in the biodiversity of the Firmicutes phylum in CD patients, particularly clostridial species. This phylogenetic group contains many bacteria that produce butyrate, a short chain fatty acid considered to have anti-inflammatory properties. Moreover, recent data suggest that clostridial species are involved in multiple regulatory processes of the innate immune system. Further research, elucidating the interactions between the gut microbiota and the immune system could potentially provide the key for understanding IBD.