Published online Nov 14, 2016. doi: 10.3748/wjg.v22.i42.9257
Peer-review started: August 14, 2016
First decision: September 12, 2016
Revised: October 7, 2016
Accepted: October 30, 2016
Article in press: October 31, 2016
Published online: November 14, 2016
Processing time: 91 Days and 10.7 Hours
The intestinal microbiome is a reservoir of microbial antigens and activated immune cells. The aims of this review were to describe the role of the intestinal microbiome in generating innate and adaptive immune responses, indicate how these responses contribute to the development of systemic immune-mediated diseases, and encourage investigations that improve the understanding and management of autoimmune hepatitis. Alterations in the composition of the intestinal microflora (dysbiosis) can disrupt intestinal and systemic immune tolerances for commensal bacteria. Toll-like receptors within the intestine can recognize microbe-associated molecular patterns and shape subsets of T helper lymphocytes that may cross-react with host antigens (molecular mimicry). Activated gut-derived lymphocytes can migrate to lymph nodes, and gut-derived microbial antigens can translocate to extra-intestinal sites. Inflammasomes can form within hepatocytes and hepatic stellate cells, and they can drive the pro-inflammatory, immune-mediated, and fibrotic responses. Diet, designer probiotics, vitamin supplements, re-colonization methods, antibiotics, drugs that decrease intestinal permeability, and molecular interventions that block signaling pathways may emerge as adjunctive regimens that complement conventional immunosuppressive management. In conclusion, investigations of the intestinal microbiome are warranted in autoimmune hepatitis and promise to clarify pathogenic mechanisms and suggest alternative management strategies.
Core tip: The intestinal microbiome is a reservoir of microbial antigens and activated immune cells that have been implicated in the pathogenesis of diverse systemic immune-mediated diseases. Dysbiosis, increased intestinal permeability, and molecular mimicry between microbial and self-antigens may initiate or sustain autoimmune hepatitis. Multiple drug, molecular, dietary, and probiotic interventions can modify the intestinal microbiome and attenuate the immune response. The role of the intestinal microbiome in autoimmune hepatitis warrants rigorous study, and new therapies may emerge that strengthen current treatment regimens.