Is a Fecal Microbiota Transplant Useful for Treating Inflammatory Bowel Disease?

Abstract

Ulcerative colitis and Crohn's disease represent the major groups of idiopathic disorders in inflammatory bowel disease (IBD). The etiology includes environmental factors, genetic factors, and immune responses. The pathogenesis is diversified; however, no guaranteed curative therapeutic regimen has been developed so far. This review contains information related to pathophysiology and current treatment options for IBD. It is known that IBD is caused by tissue-disruptive inflammatory reactions of the gut wall; that is why downregulation of the immune responses allows the healing of the damaged mucosa and allows the resetting of the physiological functions of the gut back to normal. The main treatment options are still corticosteroids, immunomodulators, antibiotics, probiotics, and a series of new agents. Their effects include modulation of cytokines, neutrophil-derived factors, adhesion molecules, and reactive oxygen/nitrogen metabolites. The monoclonal antitumor necrosis factor as infliximab recombinant anti-inflammatory cytokines or related gene therapy is also used nowadays. Still, the fecal microbiota transplantation (FMT) is considered to revolutionize the therapy in IBD, considering the abnormal inflammatory response due to the complicated relationship between microbiota and the immune system. It is imperative to mention the critical role dysbiosis may have in the pathogenesis of IBDs. This review summarizes the available literature concerning the efficacy of FMT in IBDs.

A Role for Folate in Microbiome-Linked Control of Autoimmunity

“…Overall, the gut microbiota comprises five phyla and about 160 species in the large intestine [ 33 ], and the number of genes of the intestinal microbiota is 150 times greater than the human genome [ 34 ]. Qualitative and quantitative changes in the microbial flora, their metabolic activity, and their local distribution [ 35 ] are a typical feature of IBD [ 36 ] that is otherwise characterized by the infiltration of the lamina propria with a mixed leukocyte population expressing proinflammatory cytokines [ 37 ]. Whether dysbiosis represents the cause or result of IBD (reviewed in [ 38 ]), it is a correlated biomarker of extraintestinal inflammatory disease (reviewed in [ 25 , 39 ]).…”