Chlamydia pneumoniae (C. pneumoniae) infection is associated with the initiation and progression of atherosclerosis. The migration of vascular smooth muscle cell (VSMC) from the media to the intima is a key event in the development of atherosclerosis. Interleukin-17C (IL-17C) could enhance cell migration ability. The aim of our study is to investigate the role of IL-17C in C. pneumoniae infection-promoted VSMC migration, thereby possibly accelerating atherosclerosis. We firstly demonstrated that C. pneumoniae infection significantly increased IL-17C expression in VSMCs in the atherosclerotic lesion area from ApoE deficient mice. Our in vitro study further showed that IL-17C is required for C. pneumoniae infection-promoted VSMC migration, and its expression could be regulated by c-Fos through phosphorylating extracellular signal-regulated kinase (ERK). Unexpectedly, in the present study, we also found that IL-17C is critical for C. pneumoniae infection-induced c-Fos activation. c-Fos expression and activation induced by the exposure to recombinant IL-17C were markedly suppressed in the presence of the ERK inhibitor PD98059. These results suggest a possible positive feedback between c-Fos and IL-17C after C. pneumoniae infection. Taken together, our results indicate that C. pneumoniae infection promotes VSMC migration via c-Fos/IL-17C signaling.
Keywords: Atherosclerosis; Chlamydia pneumoniae; Interleukin-17C; Migration; Vascular smooth muscle cell; c-Fos.
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