INVESTIGATION OF CD36 SCAVENGER TYPE B RECEPTOR EXPRESSING MACROPHAGES IN INTESTINAL INFLAMMATION

Abstract

<p>Currently, there is no effective cure for Inflammatory Bowel Disease (IBD), medications are aimed solely at alleviating symptoms and not curative. Great scientific efforts have been aimed at elucidating the mechanisms underlying the pathogenesis of IBD. Macrophages—antigen presenting cells—play a chief role in the pathophysiology of IBD. It has been proposed that CD36 receptor present on the surface of macrophages, may play a role in the inflamed intestine. CD36-expressing macrophages have been implicated in a variety of human diseases; however the role of CD36+ macrophages in the intestine has been limited. The aim of this study was to decipher whether or not CD36+ F4/80+ macrophages are inflammatory in the colonic intestine. Our study discovered the proportion of CD36+ F4/80+ macrophages were markedly upregulated in active IBD patients and TNBS-induced colitis mice. CD36+ macrophages isolated from the LPMC of the small and large intestine of Balb/c treatment groups(a) 12TNBS, (b) MHS+12TNBS, and (c) MHS+PA mice confirmed these macrophages expressed some level of proinflammatory cytokine TNF-α. Two macrophage ligands, LCFA: Palmitic Acid and PGN, in conjunction or separately, appeared to be two culprits which induced MHS macrophages to produce TNF-α both in vitro and in vivo. It is possible these two ligands may work in concert, however the mouse model has yet to be examined. The precise role(s) of these CD36+ F4/80+ macrophages requires further scientific inquiry and elucidation in the context of intestinal inflammation. It is quite possible understanding the mechanisms and roles of these macrophages will greatly advance our knowledge in the pathophysiology of IBD and potential therapeutic treatments or targets.</p>