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Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Chlamydia pneumoniae infection does not induce or modify atherosclerosis in mice
G Caligiuri1, M Rottenberg, A Nicoletti
1Center for Molecular Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Circulation
|June 13, 2001
Summary
Chlamydia pneumoniae (CP) infection did not induce or accelerate atherosclerosis in mouse models. Further research is needed to understand the link between CP and human coronary heart disease.
Area of Science:
- Cardiovascular Research
- Infectious Disease Research
- Atherosclerosis Pathogenesis
Background:
- Seroepidemiological studies suggest a link between Chlamydia pneumoniae (CP) and coronary heart disease (CHD).
- Experimental data indicate CP may promote or initiate atherosclerosis.
- The role of CP in atherosclerosis requires further investigation in relevant models.
Purpose of the Study:
- To evaluate the impact of CP infection on atherosclerosis development.
- To assess CP's effect in atherosclerosis-prone apolipoprotein E-knockout (apoE-KO) mice.
- To determine if CP induces atherosclerosis in wild-type mice.
Main Methods:
- Female apoE-KO and C57BL/6J mice were infected intranasally with live CP.
- Mice were maintained on a standard chow diet for 22 weeks post-infection.
- Infection confirmation via PCR and immune response assessment using ELISA.
Main Results:
- CP infection was confirmed in mouse lungs with a detectable humoral immune response.
- No significant difference in aortic atherosclerotic lesions was observed between CP-infected and control apoE-KO mice.
- CP infection did not induce atherosclerosis in wild-type C57BL/6J mice.
Conclusions:
- CP does not induce atherosclerosis in wild-type mice.
- CP does not accelerate atherosclerosis in chow-fed apoE-KO mice.
- The association between CP and human CHD remains to be clarified by future studies.

