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J Med Microbiol 55 (2006), 1017-1021; DOI: 10.1099/jmm.0.46516-0
© 2006 Society for General Microbiology
ISSN 1473-5644

Increased prostanoid dependency of arterial relaxation in Chlamydia pneumoniae-infected mice

Liisa Törmäkangas1, Juha Ketonen2, Maija Leinonen1, Pekka Saikku3 and Ilari Paakkari2

1 National Public Health Institute (KTL), PO Box 310, FIN-90101 Oulu, Finland

2 Institute of Biomedicine, University of Helsinki, Finland

3 Department of Medical Microbiology, University of Oulu, Finland

Correspondence
Liisa Törmäkangas
liisa.tormakangas{at}ktl.fi

Received 11 January 2006
Accepted 7 April 2006

Endothelial dysfunction plays an important role in the development of atherosclerosis. Previous studies have shown that inoculation with Chlamydia pneumoniae contributes to atherosclerotic development in rabbits and hypercholesterolaemic mice and causes endothelial dysfunction in apolipoprotein E-deficient mice. The effect of acute C. pneumoniae infection on endothelial function in normocholesterolaemic C57BL/6J mice was studied by measuring the force of contraction of the descending aorta after noradrenaline stimulation and in response to methacholine-induced relaxation. In addition, the effects of the nitric oxide synthase inhibitor N{omega}-nitro-L-arginine methyl ester (L-NAME) and the cyclooxygenase inhibitor diclofenac on relaxation were assessed. Pre-treatment of the aortas with L-NAME decreased the relaxation response in both the infected and uninfected groups and no significant difference was detected between these groups, whereas diclofenac significantly attenuated the relaxation response only in the infected animals. In conclusion, infection shifted the balance of endothelium-derived relaxing factors from nitric oxide towards vasorelaxing prostanoids in C57BL/6J mice.

Abbreviations: COX, cyclooxygenase; EDHF, endothelium-derived hyperpolarizing factor; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; 6-keto PGF1{alpha}, 6-keto prostaglandin F1{alpha}; MC, methacholine; L-NAME, N{omega}-nitro-L-arginine methyl ester; NO, nitric oxide; NOS, nitric oxide synthase; PGI2, prostaglandin I2.






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