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Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
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CD8+ T cells mediate Chlamydia pneumoniae-induced atherosclerosis in mice
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.
Pathogens and Disease
|July 30, 2015
Summary
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.
