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Cardiovascular Research 2005 65(2):317-327; doi:10.1016/j.cardiores.2004.09.031
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Copyright © 2004, European Society of Cardiology

Chlamydia pneumoniae infections in mouse models: relevance for atherosclerosis research

Martijn D. de Kruifa,b,*, Eric C.M. van Gorpa,b, Tymen T. Kellera, Jacobus M. Ossewaardec and Hugo ten Catea,d

aLaboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
bDepartment of Internal Medicine, Slotervaart Hospital, Amsterdam, The Netherlands
cDepartment of Medical Microbiology and Infectious Diseases, Erasmus Medical Center, Erasmus University, Rotterdam, The Netherlands
dDepartment of Internal Medicine, Academic Hospital Maastricht, University Maastricht, Maastricht, The Netherlands

* Corresponding author. Laboratory of Experimental Internal Medicine, G2-132, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. Tel.: +31 20 5667906; fax: +31 20 697 7192. Email address: m.d.dekruif{at}amc.uva.nl

Mouse models have been frequently used in the study of Chlamydia pneumoniae (also known as Chlamydophila pneumoniae) infections. This gram-negative obligate intracellular bacterium causes respiratory infections, followed by dissemination of the bacterium to various organs throughout the body, including cardiovascular tissues, supporting the current hypothesis of a relationship between C. pneumoniae and atherosclerosis. Recently, clinical trials evaluated the effect of antichlamydial antibiotics on secondary cardiovascular events. Although small studies showed some effect, the large WIZARD study did not confirm these results, and the role of antichlamydial antibiotics in prevention of secondary events was questioned. To address these issues, data obtained from mouse models were systematically reviewed here. C. pneumoniae infections showed atherogenic properties in mice that were reproducible and confirmed by different research groups. However, antibiotic therapy was of limited value in these mouse models. Antibiotic therapy effectively cleared the acute infection, but did not influence the atherogenic properties of C. pneumoniae unless the therapy was started early during the acute infection. The results summarized here may help to better understand the results of the clinical antibiotic trials.

KEYWORDS Chlamydia pneumoniae; Chlamydia psittaci strain TWAR; Chlamydophila pneumoniae; Mouse models; Mice; Cardiovascular diseases; Atherosclerosis; Antibiotics

Time for primary review 26 days


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