Is a fatty acid transporter, CD36, involved in Mycobacterium tuberculosis infection?

CD36是一种氧化LDL受体和脂肪酸转运蛋白，在各种组织和细胞中表达，包括巨噬细胞。由于结核分枝杆菌在进入巨噬细胞、细胞内生长和从溶酶体逃逸时需要脂肪酸。在本研究中，CD36在结核分枝杆菌感染人巨噬细胞中的可能作用进行了检查。来自正常和CD36阴性受试者的单核细胞衍生的巨噬细胞在体外感染结核分枝杆菌。结核分枝杆菌感染的易感性在正常和CD36阴性受试者之间没有差异。此外，抗CD36单克隆抗体对结核分枝杆菌感染巨噬细胞没有显示出显著的抑制作用。共聚焦激光显微镜没有显示任何显着的CD 36和结核分枝杆菌之间的关系。因此，本研究中未观察到CD 36与结核分枝杆菌感染之间的明确关系，但感染似乎改变了巨噬细胞脂肪酸组成，以及CD 36和PPARgamma基因的表达水平。由于这两个基因对细胞内脂肪代谢和转运有显著影响，因此CD36在结核分枝杆菌感染巨噬细胞中的可能间接作用仍有待于测试。

CD36 is an oxidized LDL receptor and a fatty acid transporter expressed in various tissues and cells, including macrophages. Since M.tuberculosis requires fatty acid in its entry into macrophages, intracellular growth, and escape from lysosomes. In the present study, possible role of CD36 in M.tuberculosis infection to human macrophages was examined. Monocyte-derived macrophages from normal and CD36-negative subjects were infected with M.tuberculosis in vitro. The susceptibility to M.tuberculosis infection was not different between normal and CD36-negative subjects. Further, monoclonal anti-CD36 antibody did not show significant suppressive effect on the infection of M.tuberculosis to macrophages. Confocal laser microscopy did not show any significant relation between CD36 and M.tuberculosis. Thus, no definite relation between CD36 and M.tuberculosis infection was observed in this stud. However, the infection appeared to change macrophageal fatty acid composition, and also the expression levels of CD36 and PPARgamma genes. Since he both genes have significant effects on intracellular fatty metabolism and transport, possible indirect role of CD36 in M.tuberculosis infection to macrophages remains to be tested.