Chlamydia pneumoniae Infection Exacerbates Atherosclerosis in ApoB100only/LDLR−/− Mouse Strain

• Published in: BioMed research international 2018-01, Vol.2018 (2018), p.1-12
• Main Authors: Burián, Katalin, Lu, Xinjie, Szabó, Andrea, Virok, Dezső Péter, Endrész, Valéria, Lantos, Ildikó, Mosolygó, Tímea
• Format: Article
• Language: English
• Subjects: Animals; Aorta; Aorta - metabolism; Aorta - pathology; Apolipoprotein E; Apolipoproteins; Apolipoproteins E - metabolism; Arteriosclerosis; Atherosclerosis; Atherosclerosis - blood; Atherosclerosis - metabolism; Atherosclerosis - pathology; Biomedical research; Cardiovascular disease; Chlamydia; Chlamydia pneumoniae; Chlamydophila Infections - metabolism; Chlamydophila Infections - pathology; Cholesterol; Disease Models, Animal; Female; Hypercholesterolemia; Hypercholesterolemia - metabolism; Hypercholesterolemia - pathology; Hyperlipidemia; Infections; Laboratories; Lipids; Lipids - blood; Lipoproteins - blood; Low density lipoprotein receptors; Male; Metabolism; Mice; Polymerase chain reaction; Receptors, LDL - metabolism; Rodents; Sampling methods; Sexually transmitted diseases; STD
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2018/8325915

Aims. Hyperlipidaemia model animals have been used to elucidate the role of Chlamydia pneumoniae (Cpn) infection in atherosclerosis. The aims of this study were to investigate the proatherogenic effect of multiple Cpn infections 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 with Cpn were subjected to morphometric analyses. Morphometric evaluation disclosed that Cpn infections 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 viable Cpn in 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 after Cpn infections; thus this mouse strain can be used as a model of infection-related atherosclerosis enhancement and can provide further evidence for the proatherogenic influence of Cpn in mice.