Extravascular inflammation does not increase atherosclerosis in apoE-deficient mice

Kerry W.S. Ko, David Corry, Cory F. Brayton, Antoni Paul, Lawrence Chan

Research output: Contribution to journalArticle

7 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)93-99
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume384
Issue number1
DOIs
StatePublished - Jun 19 2009

Keywords

  • Atherosclerosis
  • Dermatitis
  • Inflammation
  • Lung disease
  • Peritonitis

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology

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