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Implication of natural killer T cells in atherosclerosis development during a LPS‐induced chronic inflammation
Author(s) -
Ostos Maria A,
Recalde Delia,
Zakin Mario M,
Scott-Algara Daniel
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)02692-3
Subject(s) - inflammation , spleen , lipopolysaccharide , apolipoprotein b , immunology , apolipoprotein e , medicine , autoantibody , disease , endocrinology , cholesterol , antibody
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.