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Role of RANTES in the pathogenesis of experimental colitis

Platelets and platelet‐derived chemokines eg RANTES have been implicated in the pathogenesis of chronic inflammatory bowel disease (IBD). However, it remains unclear if and how platelet‐derived RANTES contributes to the blood cell recruitment and tissue injury associated with intestinal inflammation. We addressed these issues in dextran sodium sulfate (DSS)‐induced colitis in wildtype (WT) mice, WT receiving blocking antibody (mAb) to RANTES, RANTES‐deficient (RANTES−/−) mice, and RANTES−/−→WT bone marrow chimeras. Disease activity index (DAI), histopathologic injury, vascular permeability to albumin, and the adhesive interactions between leukocytes, platelets, and endothelial cells were monitored. All parameters were increased by DSS and were attenuated in RANTES−/− mice and by RANTES mAb in WT mice. A similar protection was noted in RANTES−/−→WT chimeras, suggesting that blood cells (eg, platelets) are a major source of the chemokine. Our findings implicate RANTES, likely derived from platelets, in the vascular dysfunction, inflammation, and tissue injury associated with experimental colitis, and suggest that this chemokine may be an important therapeutic target in IBD.