Abstract
Factors implicated in the pathophysiology of ulcerative colitis (UC) are an abnormal immune response, defect in intestinal epithelial barrier function, and gut microbiota. Currently, it is unclear whether specific bacterial strains are responsible for the induction of intestinal inflammation, but increased bacterial tissue invasion has been described in affected UC patients. Further, a quantitative and qualitative microbial imbalance in UC, defined as dysbiosis, has been characterized by an increase in Rhodococcus spp., Shigella spp., and Escherichia spp., but a decrease in certain Bacteroides spp.. More specifically, Campylobacter spp., Enterobacteriae, and enterohepatic Helicobacter were more prevalent in tissue sample from UC patients subjected to molecular detection methods, but not controls. In addition, serologic testing identified Fusobacterim varium as a potential contributor to the intestinal inflammation in UC. Interestingly, in-situ hybridization studies have shown anti-inflammatory Lactobacillus spp. and Pediococcus spp. were absent in samples from subjects affected by UC. Therefore, dysbiosis is a factor in the pathogenesis of UC.
Highlights
The gut microbiota consists predominantly of phyla members Bacteroidetes and Firmicutes, and to a lesser extent of Actinobacteria and Proteobacteria [1, 2]
The focus of this paper is to summarize the evidence for a role of enteric bacteria in the pathogenesis of ulcerative colitis (UC)
This study identified and implicated a novel 19.5 kDa prominent antigen in the pathogenesis of both Crohn’s disease (CD) and UC
Summary
The gut microbiota consists predominantly of phyla members Bacteroidetes and Firmicutes, and to a lesser extent of Actinobacteria and Proteobacteria [1, 2]. Genomewide association studies [12] have detected additional critical factors for the pathogenesis of UC. These include hepatocyte nuclear factor 4 (HNF4A), a protein regulating intercellular cell junctions, like desmosomes, tight and adherence junctions [13], and laminin β1 subunit (LAMB1), anchoring epithelium to the underlying basement membrane. The findings outlined above have defined the currently accepted hypothesis for the development of IBD, “Pathogenic intestinal bacteria and/or infectious agents initiate and perpetuate the inflammation of the gut through disruption of tolerance towards the commensal microbiota in an individual with genetic vulnerability.” [16]
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