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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.
Insights
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.
Background:
Seroepidemiological studies have linked Chlamydia pneumoniae (CP) to coronary heart disease, and recent experimental studies suggest that it may accelerate or even induce atherosclerosis. We therefore evaluated the effect of CP infection on atherosclerosis in atherosclerosis-prone apolipoprotein E-knockout (apoE-KO) and wild-type C57BL/6J mice.
Methods And Results:
Six- to 8-week-old female mice were infected intranasally with live CP and then fed a standard chow diet for 22 weeks. A subgroup of mice was reinfected 18 weeks after primary infection. Polymerase chain reaction analysis of lung tissue confirmed successful infection with CP, and ELISA assays demonstrated development of a humoral immune response. Despite this, no statistically significant differences in aortic atherosclerotic lesions were found between CP-infected and control apoE-KO mice. Furthermore, CP infection did not induce atherosclerosis in C57BL/6J mice.
Conclusions:
CP does not induce atherosclerosis in wild-type mice and does not accelerate atherosclerosis in chow-fed apoE-KO mice. Further studies will be necessary to clarify the explanation for the seroepidemiological association between CP and coronary heart disease in humans.
