Abstract
The intestinal epithelium forms a barrier against luminal microorganisms. Innate immunity plays a crucial role inmaintenance of that barrier, including induction of antimicrobial peptides and wound healing. In the normal mucosa, downregulation of innate immunity contributes to intestinal homeostasis. Recent genetic, serological and animal studies support dysfunction of the mucosal innate immune response tocommensal flora as a central mechanism in the pathogenesis of IBD. Toll-like receptors (TLRs) are the principal component of mucosal innate immunity. In general, the pathogenesis ofulcerative colitis and Crohn's disease may be due to increased or decreased TLR signaling, respectively. Our recent research demonstrates the possible role of TLR signaling in the development of colitis-associated neoplasia.Better understanding of the innate immune response to commensal bacteria will lead to the development of targetedand more effective therapy for patients with IBD.
| Original language | English |
|---|---|
| Title of host publication | Inflammatory Bowel Disease |
| Subtitle of host publication | Translating basic science into clinical practice |
| Publisher | Wiley-Blackwell |
| Pages | 64-81 |
| Number of pages | 18 |
| ISBN (Print) | 9781405157254 |
| DOIs | |
| State | Published - 18 May 2010 |
| Externally published | Yes |
Keywords
- Expression of Nods in health and disease
- Expression of TLRs in health and disease
- General role of TLRs and Nods - barrier function, induction of IgA and antimicrobial peptides
- Implications for therapy of IBD
- Innate immunity - implications on pathogenesis of IBD
- Innate immunity - linking genetic susceptibility to IBD and commensal bacteria
- Link between innate immunity and adaptive immunity - pathogenesis of IBD
- Overview of innate immune system