Microbial Links to Inflammatory Bowel Disease Development: Potential Interventional Strategies in TreatmentUdai P. Singh1, Narendra P. Singh1, Brandon Busbee1, Guan H1, Robert L. Price2, Dennis D. Taub3*, Manoj K. Mishra4, Mitzi Nagarkatti1 and Prakash S. Nagarkatti1
- *Corresponding Author:
- Dennis D. Taub
Laboratory of Molecular Biology and Immunology
NIA-IRP, NIH, Baltimore, MD 21224, USA
E-mail: [email protected]
Received date: September 14, 2012; Accepted date: September 18, 2012; Published date: September 22, 2012
Citation: Singh UP, Singh NP, Busbee B, Guan H, Price RL, et al. (2012) Microbial Links to Inflammatory Bowel Disease Development: Potential Interventional Strategies in Treatment. J Bacteriol Parasitol 3:151. doi: 10.4172/2155-9597.1000151
Copyright: ©2012 Singh UP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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 . 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 . 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 .