Effects of Chlamydia pneumoniae on expression of SR-A1 and CD36 in THP-1-derived macrophages and the associated signal transduction pathway / 中国免疫学杂志

ABSTRACT

Objective:To investigate the effects of Chlamydia pneumoniae(Cpn) on SR-A1 and CD36 expression in THP-1-derived macrophages and role of c-Jun NH_2-terminal signal transduction pathway in the process.Methods:Cpn was propagated in Hep-2 cells.THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA)for 48h,and were randomly allocated into four groups to be incubated continually control group;Cpn infection group;Cpn and SP600125(a JNK inhibiter)group and SP600125 group.Lipid droplets in cytoplasm were observed by oil red O staining.The contents of intracellular cholesterol ester were detected by enzyme-fluorescence.The expression of SR-A1 and CD36mRNA and protein were determined by RT-PCR and Western blot, respectively. Results:THP-1-derived macrophages infected with Cpn resulted in large accumulation of lipid droplets and foam cell formation when co-cultured with LDL.Meanwhile,the expression of SR-A1 mRNA and protein were up-regulated by Cpn infection (P<0.05).However,the expressions of CD36 mRNA and protein in THP-1-derived macrophages infected with Cpn were unchanged.Moreover,the up-regulation of SR-A1 and foam cell formation induced by Cpn could be restrained by the JNK inhibiter SP600125 in a dose-dependent manner,and SP600125 had little impact on the expression of CD36 in THP-1-derived macrophages infected with Cpn.Conclusion:The up-regulation of SR-A1 but not CD36 expression is involved in mechanisms of Cpn inducing foam cell formation.And Chlamydia pneumoniae up-regulates the expression of SR-A1 via the JNK signal transduction pathway.This may be a novel mechanism for the foam cell formation induced by Cpn.