Abstract
The exact pathogenesis of inflammatory bowel disease (IBD) is still not completely understood. It is hypothesized that a genetic predisposition leads to an exaggerated immune response to an environmental trigger, leading to uncontrolled inflammation. As there is no known causative treatment, current management strategies for inflammatory bowel disease focus on correcting the excessive immune response to environmental (including microbial) triggers. In recent years, there has been growing interest in new avenues of treatment, including targeting the microbial environment itself. Fecal microbiota transplantation (FMT) is a novel treatment modality showing promising results in early studies. The article discusses the rationale for the use of FMT in inflammatory bowel disease and the yet-unresolved questions surrounding its optimal use in practice.
Highlights
The exact pathogenesis of inflammatory bowel disease (IBD) is still not completely understood
There are more than 160 known loci associated with IBD, many of which are involved in the gut immune response, including the intestinal barrier, microbial recognition, lymphocyte regulation, and cytokine release [1,2,3]
Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria constitute more than 99% of the gut microbiota, with Firmicutes accounting for more than 60% of mucosa-attached colonic species, while Enterobacteriaceae such as Escherichia coli are a relatively minor subgroup, accounting for only 8% of all bacteria [7,8]
Summary
The exact pathogenesis of inflammatory bowel disease (IBD) is still not completely understood. There are more than 160 known loci associated with IBD, many of which are involved in the gut immune response, including the intestinal barrier, microbial recognition, lymphocyte regulation, and cytokine release [1,2,3]. Increasing incidence of IBD in both industrialized and developing countries suggests the role of some environmental factor, such as changes in diet or the microbial environment [2]. It is not known whether intestinal inflammation results from an abnormal immune response to commensal flora, or whether a primarily imbalanced gut microbiome triggers an aggressive immune response [4]. Current treatment strategies for inflammatory bowel disease focus on correcting the excessive immune response to environmental (including microbial) triggers. There has been growing interest in new avenues of treatment, including targeting the microbial environment itself [5]
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