Chlamydia pneumoniaeInfection Exacerbates Atherosclerosis in ApoB100only/LDLR−/−Mouse Strain

Abstract

Aims. Hyperlipidaemia model animals have been used to elucidate the role ofChlamydia pneumoniae (Cpn)infection in atherosclerosis. The aims of this study were to investigate the proatherogenic effect of multipleCpninfections in ApoB100only/LDLR−/−mice which based on lipid profile can be regarded as the most suitable mouse model of human hypercholesterolemia and to compare the lesion development to that in a major atherosclerosis model ApoE−/−mice.Methods and Results. Aorta samples of ApoB100only/LDLR−/−mice infected three times withCpnwere subjected to morphometric analyses. Morphometric evaluation disclosed thatCpninfections exacerbated atherosclerosis development in the aortic root and descending aorta of the mice fed with normal diet. Viable Cpn was detected in the ascending aorta by RT-PCR. Chlamydial 16SrRNA expression showed the presence of viableCpnin the aorta of infected animals. A similar rate of acceleration of atherosclerosis was observed when the infection protocol was applied in ApoB100only/LDLR−/−and in ApoE−/−mice.Conclusion. Similar to ApoE−/−mice, ApoB100only/LDLR−/−mice with more human-relevant serum lipoprotein composition develop increased atherosclerosis afterCpninfections; thus this mouse strain can be used as a model of infection-related atherosclerosis enhancement and can provide further evidence for the proatherogenic influence ofCpnin mice.