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Mouse models of C. pneumoniae infection and atherosclerosis
L A Campbell1, E Blessing, M Rosenfeld
1Department of Pathobiology, University of Washington, Seattle, WA 98195, USA.
Abstract:
Mouse models were used to determine whether Chlamydia pneumoniae establishes chronic infection of the aorta and contributes to atherogenesis. Persistent infection of the aorta occurred in 11 of 31 hyperlipidemic apolipoprotein E-deficient (apoE(-/-)) mice but not in C57BL/6J mice fed a normal diet after a single inoculation and in both models following repeated inoculation with C. pneumoniae. Repeated inoculation of C57BL/6J mice resulted in inflammatory changes in the heart and aorta in 8 of 40 of mice; however, no atherosclerotic lesion development was observed. Repeated inoculation of apoE(-/-) mice resulted in a statistically significant increase in lesion area (n=43; P=.05). Although Chlamydia trachomatis disseminated to the aorta, persistent infection was not established and no statistically significant increase in lesion area occurred. These studies suggest that persistent infection of the aorta can lead to inflammatory changes in the absence of hyperlipidemia and accelerate lesion progress in concert with hyperlipidemia.
Insights
Chlamydia pneumoniae can cause chronic aortic infection, contributing to atherosclerosis in hyperlipidemic mice. This persistent infection accelerates lesion development, highlighting its role in cardiovascular disease progression.
Area of Science:
- Cardiovascular Science
- Infectious Disease Research
- Atherosclerosis Pathogenesis
Background:
- Chlamydia pneumoniae is a potential contributor to atherosclerosis.
- Understanding its role in chronic aortic infection and atherogenesis is crucial.
Purpose of the Study:
- To investigate if Chlamydia pneumoniae establishes chronic aortic infection.
- To determine its contribution to atherogenesis in mouse models.
Main Methods:
- Utilized hyperlipidemic apolipoprotein E-deficient (apoE(-/-)) mice and C57BL/6J mice.
- Administered single and repeated inoculations of C. pneumoniae.
- Assessed aortic infection, inflammation, and atherosclerotic lesion development.
Main Results:
- Persistent aortic infection with C. pneumoniae occurred in 11/31 hyperlipidemic apoE(-/-) mice.
- Repeated inoculation in apoE(-/-) mice led to a significant increase in lesion area (P=.05).
- C. trachomatis disseminated but did not establish persistent infection or increase lesion area.
Conclusions:
- Persistent Chlamydia pneumoniae infection of the aorta can induce inflammation, even without hyperlipidemia.
- This infection accelerates atherosclerotic lesion progression in the presence of hyperlipidemia.
- Chlamydia pneumoniae is implicated in the pathogenesis of atherosclerosis.