细菌学与寄生虫学杂志

抽象的

Microbial Links to Inflammatory Bowel Disease Development: Potential Interventional Strategies in Treatment

Udai P. Singh, Narendra P. Singh, Brandon Busbee, Guan H, Robert L. Price, Dennis D. Taub, Manoj K. Mishra, Mitzi Nagarkatti and Prakash S. Nagarkatti

The two major forms of Inflammatory Bowel Disease (IBD), Crohn’s disease (CD) and ulcerative colitis (UC), affect an estimated 3.6 million people globally [1]. The main mechanisms responsible for the induction and pathogenesis of IBD remain unknown, but there is a general agreement, those intestinal microbiotas that mediate dysregulation of the immune system resulting in progression and development of IBD, are involved [2]. More recent studies have demonstrated that luminal antigens play an active role, to mediate mucosal immune responses that induce IBD progression. In humans, inflammation is most severe in the part of the gut that contains the highest bacterial concentration [3,4]. It is well known that mice fail to develop colitis or have a reduced severity under germ-free conditions, suggesting a pathologic connection between immune cells and commensal enteric bacteria to develop IBD [5-8]. Due to prolonged mucosal contact in parts of the ileum, rectum and caecum regions, the pathogenic germ(s) may decrease the protective bacteria that induce mucosal permeability and lead to enhanced exposure of bacterial products to Toll-like receptors (TLR), and antigens that directly activate the pathogenic T cell immune responses to induce IBD. This induction also mediates regulatory T cell dysfunction or antigen-presenting cells (APC) that might lead to further decreased tolerance to microbial antigens [9].