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Introduction

Inflammatory bowel disease (IBD) is a chronic illness that results from the impaired regulation of inflammation in the mucosal layers of the intestines [1]. There are two forms of IBD: Crohn’s disease (CD) and ulcerative colitis (UC) [2]. The study of IBD pathogenesis is becoming increasingly important as its incidence is highest in North America and is increasing worldwide (Figure 1) [3]. It has been found that genetics, environmental factors, and the composition of normal flora may increase the susceptibility of individuals to IBD [2][4]. Pathogenic Escherichia coli is a known bacterial cause of IBD. The microbial mechanisms of certain E. coli strains enhance their pathogenicity, which contribute to the initiation and development of IBD [5] [6]. Furthermore, the interactions between commensal bacteria of the normal flora and host cells contribute to the chronicity of IBD [5].