Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

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

Liuba, Petru LU ; Karnani, P ; Pesonen, Erkki LU ; Paakkari, I ; Forslid, Anders LU orcid ; Johansson, Leif LU ; Persson, Kenneth LU ; Wadström, Torkel LU and Laurini, Ricardo LU (2000) In Circulation 102(9). p.1039-1044
Abstract
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... (More)
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. (Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Circulation
volume
102
issue
9
pages
1039 - 1044
publisher
Lippincott Williams & Wilkins
external identifiers
  • pmid:10961970
  • scopus:0034730095
ISSN
1524-4539
language
English
LU publication?
yes
additional info
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)
id
130c865f-0eb1-4bd0-88ca-fe876b492ec5 (old id 1117769)
alternative location
http://circ.ahajournals.org/cgi/content/abstract/102/9/1039
date added to LUP
2016-04-01 15:47:23
date last changed
2022-03-22 06:11:45
@article{130c865f-0eb1-4bd0-88ca-fe876b492ec5,
  abstract     = {{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:&lt;0.05 and P:&lt;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:&lt;0.05) but not in noninfected mice. The relaxation response from infected mice tended to differ in the same manner at 6 weeks (P:&lt;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.}},
  author       = {{Liuba, Petru and Karnani, P and Pesonen, Erkki and Paakkari, I and Forslid, Anders and Johansson, Leif and Persson, Kenneth and Wadström, Torkel and Laurini, Ricardo}},
  issn         = {{1524-4539}},
  language     = {{eng}},
  number       = {{9}},
  pages        = {{1039--1044}},
  publisher    = {{Lippincott Williams & Wilkins}},
  series       = {{Circulation}},
  title        = {{Endothelial dysfunction after repeated Chlamydia pneumoniae infection in apolipoprotein E-knockout mice}},
  url          = {{http://circ.ahajournals.org/cgi/content/abstract/102/9/1039}},
  volume       = {{102}},
  year         = {{2000}},
}