Premium
CD36, fibroblasts and intestinal inflammation
Author(s) -
Reaves Titus,
Nillas Andrea,
AndersonThomas Megan
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.142.2
Subject(s) - cd36 , inflammation , fibrosis , fibroblast , scavenger receptor , immune system , receptor , immunology , biology , medicine , chemistry , pathology , endocrinology , in vitro , biochemistry , lipoprotein , cholesterol
Crohn's Disease (CD) is characterized by dysregulated intestinal inflammation with an unknown etiology. Intestinal fibrosis is a major pathophysiological complication of CD with features that include an overproduction of collagen, excessive contraction of intestine tissue, and intestinal stricture. Fibroblasts are mesenchymal cells that produce the excess collagen resulting in the aforementioned fibrosis. We have shown that intestinal fibroblasts express a variety of immune receptors. A reduction in CD36 (membrane‐bound and scavenger receptor that is an indicator of inflammation and interacts with TLR‐2, 4, and 6) on the surface of fibroblast results in a statistically significant reduction in transmigration of polymorphonuclear leukocytes (PMN) toward such fibroblasts. Dextran sodium sulfate (DSS) was administered to CD36‐deficient mice and age‐matched controls; DSS typically results in intestinal inflammation that is similar to that observed in Crohn's Disease. Results indicated that mouse PMN were less vigorous in their capacity to migrate toward fibroblasts and there was less inflammation observed in both the large and small intestine of CD36‐deficient mice. Results suggest that CD36 may play a prominent role in the inflammatory responses of fibroblasts in the intestine and highlight CD36 as a potential target receptor in the treatment of aberrant mucosal inflammation, which leads to fibrosis.