Interleukin-10 deficiency increases atherosclerosis, thrombosis, and low-density lipoproteins in apolipoprotein E knockout mice

Mol Med. 2003 Jan-Feb;9(1-2):10-7.

Abstract

Interleukin (IL)-10 is an anti-inflammatory cytokine that may play a protective role in atherosclerosis. The aim of this study was to assess the effect of IL-10 deficiency in the apolipoprotein E knockout mouse. Apolipoprotein E deficient (E-/-) and IL-10 deficient (-/-) mice were crossed to generate E-/- x IL-10-/- double knockout mice. By 16 wk, cholesterol and triglycerides were similar in double and single knockouts but the lack of IL-10 led to increased low-density lipoprotein cholesterol whereas very-low-density lipoprotein was reduced. In parallel, T-helper 1 responses and lesion size were dramatically increased in double knockout compared with E-/- controls. At 48 wk, matrix metalloproteinases and tissue factor activities were increased in lesions of double-knockout mice. Furthermore, markers of systemic coagulation were increased, and vascular thrombosis in response to i.v. thrombin occurred more frequently in E-/- x IL-10-/- than in E-/- mice. Our findings suggest that IL-10 deficiency plays a deleterious role in atherosclerosis. The early phase of lesion development was increased, and the proteolytic and procoagulant activity was elevated in advanced lesions. These data show that IL-10 may reduce atherogenesis and improve the stability of plaques.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apolipoproteins E / deficiency
  • Apolipoproteins E / physiology*
  • Arteriosclerosis / etiology*
  • Arteriosclerosis / genetics
  • Arteriosclerosis / metabolism
  • Blood Coagulation / physiology
  • Crosses, Genetic
  • Diet, Atherogenic
  • Interleukin-10 / deficiency
  • Interleukin-10 / physiology*
  • Lipoproteins, LDL / metabolism*
  • Lipoproteins, VLDL / metabolism
  • Matrix Metalloproteinases / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Phenotype
  • Receptors, LDL / metabolism
  • Th1 Cells / immunology
  • Th2 Cells / immunology
  • Thrombosis / etiology*
  • Thrombosis / genetics
  • Thrombosis / metabolism

Substances

  • Apolipoproteins E
  • Lipoproteins, LDL
  • Lipoproteins, VLDL
  • Receptors, LDL
  • Interleukin-10
  • Matrix Metalloproteinases