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Cardiovascular Research 2002 56(2):269-276; doi:10.1016/S0008-6363(02)00544-8
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Chlamydophila pneumoniae (Chlamydia pneumoniae) accelerates the formation of complex atherosclerotic lesions in Apo E3-Leiden mice

R Ezzahiria,*, H.J.M.G Nelissen-Vranckenb, H.A.J.M Kurversa, F.R.M Stassenb, I Vliegenb, G.E.L.M Graulsb, M.M.L van Pula,b, P.J.E.H.M Kitslaara and C.A Bruggemanb

aDepartment of Surgery, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 5800, 6202 AZ Maastricht, The Netherlands
bDepartment of Medical Microbiology, Cardiovascular Research Institute Maastricht, Maastricht University, PO Box 5800, 6202 AZ Maastricht, The Netherlands

rajaa_ezzahiri{at}hotmail.com

* Corresponding author. Tel.: +31-43-387-6644; fax: +31-43-387-6643.

Objective: Atherosclerosis is an inflammatory process and is characterised by the presence of T-lymphocytes in the lesions. To study the role of Chlamydophila pneumoniae (C. pneumoniae) in this process and the effect of infection on T-cell influx, we infected Apo E3-Leiden mice with C. pneumoniae and investigated the effect on lesion development and T-cell influx in atherosclerotic lesions at different time points post infection (pi). Methods: Nine week old mice, fed an atherogenic diet, were either mock-infected or infected with C. pneumoniae and sacrificed at 1, 6 and 9 months pi. Longitudinal sections of the aortic arches of the mice were stained with hematoxylin–eosin for atherosclerotic lesion type and lesion area analysis, or with rabbit-anti-CD3+ to detect the presence of T-cells in the atherosclerotic lesions. T-cell influx was expressed as number of T-lymphocytes/lesion area. Results: At 1 month pi, type 1, 2 and 3 lesions were present. At other time points pi, more complex lesion types 4, 5a and 5b were also present. Although infection did not influence the total lesion number or area, we observed an effect of C. pneumoniae infection on lesion type. Infection resulted in a significant shift in lesion formation from type 3 to type 4 (P=0.022) at 6 months pi, and from type 4 to type 5a (P=0.002) at 9 months pi. T-cells were observed at every time point pi. At 1 month pi, a significant increase in T-cell influx in the C. pneumoniae-infected atherosclerotic lesions was observed (P=0.0005). Conclusion: This study shows that C. pneumoniae infection enhances the inflammatory process by increasing T-lymphocytes in the plaque and accelerates the formation of complex lesions.

KEYWORDS Atherosclerosis; Immunology; Infection/inflammation; Leukocytes; Macrophages


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