CD8+ T cells mediate Chlamydia pneumoniae-induced atherosclerosis in mice
Related Experiment Video
Updated: Apr 6, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Mark T Zafiratos1, Srikanth Manam2, Kyle K Henderson3
1Department of Pathology, Midwestern University, Downers Grove, IL 60515, USA Department of Biomedical Sciences, Midwestern University, Downers Grove, IL 60515, USA.
Insights
CD8(+) T cells worsen atherosclerosis exacerbated by Chlamydia pneumoniae infection. Removing these T cells reduced plaque development in mice, indicating their critical role in this condition.
Area of Science:
- Immunology
- Cardiovascular Research
- Infectious Diseases
Background:
- Chlamydia pneumoniae infection is linked to atherosclerosis exacerbation.
- CD8(+) T cells are implicated in immune responses to pathogens.
Purpose of the Study:
- To investigate the role of CD8(+) T cells in Chlamydia pneumoniae-induced atherosclerosis using a mouse model.
Main Methods:
- Wild-type (WT) and CD8α gene-deficient (CD8 KO) C57BL/6J mice were infected with C. pneumoniae and fed a high-fat diet.
- Atherosclerotic plaque development was assessed at day 100.
- CD8 KO mice were repleted with WT CD8(+) T cells to evaluate their impact.
Main Results:
- Infected CD8 KO mice showed significantly reduced atherosclerotic lesions compared to infected WT mice.
- Serum antibody response and cholesterol levels were similar between infected groups.
- Repletion of CD8 KO mice with CD8(+) T cells restored lesion development to WT levels.
Conclusions:
- CD8(+) T cells are crucial mediators in the exacerbation of atherosclerosis by Chlamydia pneumoniae.
- Targeting CD8(+) T cell responses may offer a therapeutic strategy for C. pneumoniae-associated cardiovascular pathology.
Abstract:
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 × 10(7) 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.
