Implication of natural killer T cells in atherosclerosis development during a LPS‐induced chronic inflammation

FEBS Letters

Zakin, Mario M²  Ostos, Maria A²  Recalde, Delia²  Scott-Algara, Daniel¹ 

[1]Unité d'Immuno-Hématologie et d'Immunopathologie, Institut Pasteur, 25 rue du docteur Roux, 75724 Paris Cedex 15, France

[2]Unité d'Expression des Gènes Eucaryotes, Institut Pasteur, Paris, France

关键词: Rodent;    Th1/Th2 cells;    Lipopolysaccharide;    Inflammation;    Knockout;    MAD;    malondialdehyde;    apoE0;    apolipoprotein E-deficient mice;    oxLDL;    oxidized low-density lipoprotein;    NK-T;    natural killer T cell;   

DOI  :  10.1016/S0014-5793(02)02692-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Atherosclerosis has many features of a chronic inflammatory disease. To evaluate the role of lipopolysaccharide (LPS), mimicking a systemic infection, we administered the endotoxin to apolipoprotein E (apoE)-deficient mice. LPS injections increase the atherosclerotic lesion size and the titer of plasma autoantibodies directed against oxidized low-density lipoprotein. We found that Th1 and Th2 T cells help the activation of B cells in the autoimmune response. The number of interleukin-4 producing natural killer T cells is highly increased in peripheral blood, liver, spleen and thymus cells, as well as in the atherosclerotic plaque of the LPS-treated mice. Finally, an important adventitial infiltrate of activated lymphocytes, sign of an advanced atherosclerosis, is observed only in the LPS-treated mice. Our results demonstrate that LPS administration aggravates atherosclerosis in apoE-deficient mice. LPS-injected apoE-deficient mice appear to be an excellent animal model to analyze the implementation of new therapeutic approaches in the treatment of atherosclerosis by manipulating immunological effectors.

【 授权许可】

Unknown