Role of tumor necrosis factor-α and glucocorticoid on lipopolysaccharide (LPS)-induced apoptosis of thymocytes |
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Authors: | Y Kato A Morikawa T Sugiyama N Koide G-Z Jiang K Takahashi T Yokochi |
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Institution: | Department of Microbiology and Immunology, Aichi Medical University, Nagakute, Aichi 480-11, Japan |
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Abstract: | Abstract Administration of bacterial lipopolysaccharide (LPS) into mice markedly induced the apoptosis of CD4+8+ thymocytes. The injection of anti-tumor necrosis factor (TNF)-α antibody or RU38486, a glucocorticoid receptor antagonist, into mice definitely inhibited LPS-induced apoptosis of thymocytes. Addition of the sera 1 h after injection of LPS into in vitro cultures of thymocytes caused thymocyte apoptosis. It was also prevented by either anti-TNF-α antibody or RU38486. Further, recombinant TNF-α and hydrocortisone collaborated in induction of the thymocyte apoptosis in vitro. The in vivo phenomenon of LPS-induced apoptosis of thymocytes was reproducible by the in vitro experimental system. It was therefore suggested that both TNF-α and glucocorticoid participate and collaborate as effector molecules in LPS-induced apoptosis of thymocytes. |
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Keywords: | Lipopolysaccharide TNF-α Glucocorticoid Apoptosis Thymocyte |
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