CD8+ T cells mediate Chlamydia pneumoniae-induced atherosclerosis in mice

Chlamydia pneumoniae is a community-acquired bacterial pathogen that has been strongly associated with exacerbation of atherosclerosis. We evaluated the role of CD8+ T cells in the C57BL/6J mouse model of C. pneumoniae-induced atherosclerosis. Groups of 4- to 6-week-old male wild-type C57BL/6J (WT) mice and mice with a gene deficiency in CD8α (CD8 KO mice) were infected with C. pneumoniae and fed a high fat (HF) diet. Serum antibody response and serum cholesterol were comparable between infected CD8 KO and WT mice. However, infected CD8 KO mice displayed significantly reduced atherosclerotic plaque lesions on day 100 compared to infected WT mice, at a level comparable to both uninfected WT and CD8 KO mice fed the HF diet. Moreover, repletion of CD8 KO mice with WT CD8+ T cells (1 × 107 cells/mouse intravenously) at the time of infection reverted atherosclerotic plaque lesions to WT levels. These results demonstrate that CD8+ T cells play an important role in mediating C. pneumoniae-induced exacerbation of atherosclerotic pathology. This study uses the mouse model to demonstrate the role of CD8 T cells, an immune cell type, in causation of cardiovascular diseases by the human pathogen Chlamydia pneumoniae.