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

详细信息    查看全文

• 作者：Ostos ; Maria A. ; Recalde ; Delia ; Zakin ; Mario M. ; Scott-Algara ; Daniel
• 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
• 刊名：FEBS Letters
• 出版年：2002
• 出版时间：May 22, 2002
• 年：2002
• 卷：519
• 期：1-3
• 页码：23-29
• 全文大小：477 K

文摘

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.