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BioMed Research International
Volume 2018 (2018), Article ID 8325915, 12 pages
Research Article

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

1Department of Medical Microbiology and Immunobiology, University of Szeged, Dóm Tér 10, Szeged 6720, Hungary
2Institute of Surgical Research, University of Szeged, Szőkefalvi-Nagy Béla U. 6, Szeged 6720, Hungary
3The Mary and Garry Weston Molecular Immunology Laboratory, Thrombosis Research Institute, Emmanuel Kaye Building, Manresa Road, London SW3 6LR, UK

Correspondence should be addressed to Valéria Endrész; uh.degezs-u.dem@airelav.zserdne

Received 14 November 2017; Revised 31 January 2018; Accepted 18 February 2018; Published 25 March 2018

Academic Editor: Daniele Corsaro

Copyright © 2018 Ildikó Lantos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.