Document Detail


Nitric oxide synthase plays a role in Chlamydia pneumoniae-induced atherosclerosis.
MedLine Citation:
PMID:  14522420     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Chlamydia pneumoniae infection has been associated with atherosclerosis, although the mechanisms by which C. pneumoniae contribute to atherogenesis remain unclear. Altered production of nitric oxide, a known bactericidal and anti-inflammatory agent, represents one possible mechanistic link. To examine this issue, a diet-induced, hyperlipidemic mouse model of early atherosclerosis was used. METHODS: A series of intranasal inoculations of C. pneumoniae strain AR-39 were administered to mice lacking endothelial or inducible nitric oxide synthase and to normal controls. After 18 weeks on an atherogenic diet, atherosclerotic lesion area in the aortic sinus was measured using computer-assisted morphometry. RESULTS: In the absence of C. pneumoniae infection, diet-fed eNOS(-/-) mice developed enlarged fatty streak lesions of borderline significance in comparison to uninfected, wild-type mice, while the lesion area in uninfected, diet-fed iNOS(-/-) mice did not differ significantly from lesion area in wild-type animals. In contrast, lesion area in infected eNOS(-/-) mice increased slightly, but not significantly in comparison to uninfected eNOS(-/-) mice. Lesion area in the infected iNOS(-/-) mice was significantly enlarged when compared to both uninfected iNOS(-/-) mice as well as to infected wild-type mice. CONCLUSIONS: These data suggest that production of nitric oxide by eNOS protects against development of fatty streak lesions in uninfected hyperlipidemic mice, but does not offer additional protection in infected hyperlipidemic mice, while iNOS may play a protective role, thus limiting chlamydial exacerbation of fatty streak lesions.
Authors:
Brian B Chesebro; Erwin Blessing; Cho-Chou Kuo; Michael E Rosenfeld; Mirja Puolakkainen; Lee Ann Campbell
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cardiovascular research     Volume:  60     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2003 Oct 
Date Detail:
Created Date:  2003-10-02     Completed Date:  2003-12-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  170-4     Citation Subset:  IM    
Affiliation:
Department of Pathobiology, University of Washington, P.O. Box 357238, Seattle, WA 98195, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Chlamydia Infections / enzymology*
Chlamydophila pneumoniae*
Coronary Disease / enzymology*,  microbiology*
Hyperlipidemias / enzymology,  microbiology
Male
Mice
Mice, Inbred C57BL
Models, Animal
Nitric Oxide Synthase / metabolism,  physiology*
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Grant Support
ID/Acronym/Agency:
HL-56036/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos2 protein, mouse; EC 1.14.13.39/Nos3 protein, mouse

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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