Many patients with Crohn's disease have alterations in NOD2 - a molecule that senses the presence of pathogenic bacteria.
Dr Warren Strober and colleagues examined a mouse model for human Crohn's disease.
They found that NOD2 normally inhibits the inflammation process initiated by toll-like receptors on the surface of gut cells. The toll-like receptors alert the host to the presence of pathogenic bacteria.
|NOD2 normally inhibits the inflammation process.|
However, mice without NOD2, or those with NOD2 alterations similar to those found in patients with Crohn's disease, had increased toll-like-receptor- 2-mediated inflammation.
Alterations in NOD2 may leave patients with Crohn's disease no way to turn off the inflammation that normally occurs when the gut confronts pathogens.
This new understanding of how inflammation is modulated provides a potential molecular target for dampening inflammation of the gut.