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. 1. Introduction The gut microbiota consists predominantly of phyla members Bacteroidetes and Firmicutes, and to a lesser extent of Actinobacteria and Proteobacteria [1, 2]. There is an estimated 500 to 1,000 different bacterial species represented throughout the human intestine [3]. The number of colony forming units has been calculated at a range from 1013 to 1014, exceeding the number of human cells by factor of 10 [4]. The enteric bacterial flora as a whole is essential to the normal development and function of the intestine. Salvage of unabsorbed carbohydrates, converted into short-chain fatty acids by bacterial enzymes, is an essential energy source for intestinal epithelial cell and barrier function. The colonic microflora is also central to the synthesis of vitamins B and K [5], and maintenance of intestinal innate and adaptive immune response [3]. On the other side, there is mounting evidence that the intestinal microflora can induce, transfer, and prevent conditions like obesity, type I diabetes, and inflammatory bowel disease (IBD) with a detrimental effect on human health [6]. The focus of this paper is to summarize the evidence for a role of enteric bacteria in the pathogenesis of ulcerative colitis (UC). Computational data mining by canonical correlation analysis confirmed the critical and disease-relevant interaction of mucosa-associated bacteria and host in IBD [7]. Bacterial interactions with the
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