Send to:

Choose Destination
See comment in PubMed Commons below
Curr Opin Gastroenterol. 2008 Jul;24(4):448-54. doi: 10.1097/MOG.0b013e3282ff8b0c.

Innate immunity in inflammatory bowel disease: state of the art.

Author information

  • 1Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.



Gut is exposed to enteric bacteria and food antigens but maintains its homeostasis without the development of acute or chronic inflammation in normal situations. Abnormal innate immunity to enteric flora may develop into intestinal inflammation such as inflammatory bowel disease. This paper reviews recent studies on innate immunity in gut homeostasis and inflammation, identifying novel susceptible genes and clarifying the interaction between epithelial cells and immune cells such as intestinal macrophages and dendritic cells, as well as the interaction between NOD2 and toll-like receptor.


Crosstalk between epithelial cells and monocytic cells such as macrophages and dendritic cells plays an important role in gut homeostasis. Dysregulation of this crosstalk leads to decreased epithelial integrity and chronic intestinal inflammation. Macrophages and dendritic cells also regulate bacterial flora for the maintenance of intestinal homeostasis. Interleukin-23 derived from these cells is a key cytokine in inflammatory bowel disease pathogenesis. Interactions between NOD2 and toll-like receptor signaling pathways may cause abnormal immune responses and decreased bacterial clearance. Genome-wide scanning has identified innate immunity-related genes as inflammatory bowel disease susceptibility genes.


Recent studies on gut innate immunity in animal models have greatly advanced our knowledge of inflammatory bowel disease pathogenesis. For further progress, human studies and clarification of the functions of the identified susceptibility genes are needed.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins
    Loading ...
    Write to the Help Desk