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    Biochem Biophys Res Commun. 2009 Jun 19;384(1):93-9. Epub 2009 Apr 22.

    Extravascular inflammation does not increase atherosclerosis in apoE-deficient mice.

    Ko KW, Corry DB, Brayton CF, Paul A, Chan L.

    Source

    Department of Molecular & Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.

    Abstract

    There is much speculation whether extravascular inflammation accelerates atherosclerosis. We tested this hypothesis in apoE(-/-) mice using three well-characterized models of non-autoimmune chronic inflammation: croton oil-induced skin inflammation, Aspergillus fumigatus antigen-induced allergic lung disease, and A. fumigatus antigen-induced peritonitis. The croton oil model produced recurrent inflammatory skin ulceration, and marked increases in plasma levels of IL-6 and serum amyloid A (SAA). The allergic lung disease model showed strong local inflammation with eosinophilic infiltration and serum IgE induction. The recurrent peritonitis model was accompanied by mild elevation in plasma SAA levels. Aortic atherosclerosis was quantified by computer-assisted morphometry of en face arteries in apoE(-/-) mice at 34 weeks for the croton oil model, 26 and 42 weeks for the allergic lung disease model, and 26 weeks for the peritonitis model. We found that all three forms of chronic extravascular inflammation had no effect on the rate of atherosclerosis development.

    PMID:
    19393222
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC2739567
    Free PMC Article

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