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Infection and Immunity, October 2005, p. 6458-6466, Vol. 73, No. 10
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.10.6458-6466.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Effects of Repeated Chlamydia pneumoniae Inoculations on Aortic Lipid Accumulation and Inflammatory Response in C57BL/6J Mice{dagger}

Liisa Törmäkangas,1* Leena Erkkilä,1 Taina Korhonen,2 Terttu Tiirola,3 Aini Bloigu,1 Pekka Saikku,2 and Maija Leinonen1

National Public Health Institute, Oulu, Finland,1 Department of Medical Microbiology, University of Oulu, Oulu, Finland,2 National Public Health Institute, Helsinki, Finland3

Received 10 March 2005/ Returned for modification 21 April 2005/ Accepted 1 June 2005

Chlamydia pneumoniae is a common respiratory tract pathogen, and persistent infections have been associated with atherosclerosis. We studied the effects of repeated chlamydial inoculations on the inflammatory response and on aortic lipid accumulation in C57BL/6J mice. Mice fed a diet supplemented with 0.2% cholesterol were infected three or six times with C. pneumoniae every fourth week. Sera and lungs were analyzed for inflammatory responses, lung tissues were tested for the presence of C. pneumoniae DNA and RNA, and intimal lipid accumulation in the aortic sinus was quantified. High levels of chlamydial heat shock protein 60 (Hsp60) immunoglobulin G2c subclass antibodies were detected in all of the infected mice, and a positive and statistically significant correlation was found between these antibodies and autoantibodies against mouse Hsp60. Both Hsp60 antibody levels correlated with the severity of lung tissue inflammation. The cholesterol supplement in the diet had no effect on serum cholesterol levels. Significantly larger intimal lipid lesions were seen in the mouse group infected six times (6,542 µm2) than in the control group (1,376 µm2; P = 0.034). In conclusion, repeated inoculations increased aortic sinus lipid accumulation in normocholesterolemic mice. The correlation between the antibodies to mouse and chlamydial Hsp60 proteins and their association with lung inflammation further support the theory of the development of an autoimmune response against heat shock proteins after repeated chlamydial infections.

* Corresponding author. Mailing address: National Public Health Institute, PL 310, FIN-90101 Oulu, Finland. Phone: 358-8-5376231. Fax: 358-8-5376251. E-mail: liisa.tormakangas{at}ktl.fi.

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Editor: J. N. Weiser

Infection and Immunity, October 2005, p. 6458-6466, Vol. 73, No. 10
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.10.6458-6466.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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