JCI table of contents: May 22, 2008(o:fgao@gladstone.ucsf.edu fgao@gladstone...),Health

View the PDF of this article at: https://www.the-jci.org/article.php?id=35662

Although Crohn disease (CD) and ulcerative colitits (UC) are both types of inflammatory bowel disease (IBD), the mechanisms underlying these two diseases are different. New insight into the inflammatory cell disturbances in the intestines of individuals with CD has been provided by Toshifumi Hibi and colleagues, at Keio University School of Medicine, Japan, who have suggested that these changes might contribute to the development of disease.

Most immune cells known as macrophages that live in the intestine do not express the molecule CD14 and this characteristic is associated with a lack of production of proinflammatory factors known as cytokines. In the study, an increased number of macrophages expressing CD14 (as well as other molecules not usually expressed by intestinal macrophages) were detected in the intestines of individuals with CD compared with the intestines of healthy individuals and those with UC. These cells produced large amounts of the proinflammatory cytokines IL-23 and TNF-alpha, which caused other immune cells in the area to produce another proinflammatory cytokine, IFN-gamma. As the IFN-gamma was found to cause a further increase in the number of macrophages expressing CD14 and producing IL-23, the authors suggest that IL-23 and IFN-gamma form a positive feedback loop that promotes inflammation in the intestine of individuals with CD.

TITLE: Unique CD14+ intestinal macrophages contribute to the pathogenesis of Crohn disease via IL-23/IFN-gamma axis

AUTHOR CONTACT:
Toshifumi Hibi
Keio University School of Medicine, Tokyo, Japan.
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