Endothelial dysfunction after repeated Chlamydia pneumoniae infection in apolipoprotein E-knockout mice

Petru Liuba, P Karnani, Erkki Pesonen, I Paakkari, Anders Forslid, Leif Johansson, Kenneth Persson, Torkel Wadström, Ricardo Laurini

Research output: Contribution to journalArticlepeer-review


BACKGROUND: Arterial relaxation is largely regulated by endothelial nitric oxide (NO). Its diminished activity has been associated with incipient atherosclerosis. We investigated the endothelium-dependent relaxation of aorta in apolipoprotein E-knockout (apoE-KO) mice exposed to single or repeated Chlamydia pneumoniae inoculation. METHODS AND RESULTS: Forty-eight apoE-KO mice, 8 weeks old, were inoculated intranasally with C pneumoniae (n=24) or saline (n=24) every 2 weeks over a 6-week period. Twenty mice (10 infected and 10 controls) were killed at 2 weeks and 6 weeks, respectively, after the first inoculation. The smooth muscle tone of aortic rings was measured in vitro at both time points. The norepinephrine-precontracted thoracic aortic rings were successively exposed to methacholine in the absence and presence of N:(G)-nitro-L-arginine methyl ester (L-NAME) and diclofenac. The methacholine-induced relaxation was attenuated in the infected mice at 6 weeks in both the absence and presence of L-NAME (P:<0.05 and P:<0.01, respectively). When administered together with L-NAME, diclofenac enhanced the relaxation of the L-NAME-pretreated aortas in infected mice at 2 weeks (P:<0.05) but not in noninfected mice. The relaxation response from infected mice tended to differ in the same manner at 6 weeks (P:<0.1). No intimal thickening was detected at either time point. CONCLUSIONS: C pneumoniae impairs arterial endothelial function, and the NO pathway is principally involved. Cyclooxygenase-dependent vasoconstricting products may also account for the infection-induced impaired relaxation. These findings further support the role of C pneumoniae infection in atherosclerosis development.
Original languageEnglish
Pages (from-to)1039-1044
Issue number9
Publication statusPublished - 2000

Bibliographical note

The information about affiliations in this record was updated in December 2015.
The record was previously connected to the following departments: Division of Medical Microbiology (013250400), Lab Animal Science (013100004), Pathology, (Lund) (013030000), Clinical Microbiology, Malmö (013011000), Paediatrics (Lund) (013002000), Department of Obstetrics and Gynaecology (Lund) (013018000)

Subject classification (UKÄ)

  • Cardiac and Cardiovascular Systems


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