首页> 美国卫生研究院文献>Infection and Immunity >Staphylococcal toxic shock syndrome toxin 1-induced tumor necrosis factor alpha and interleukin-1 beta secretion by human peripheral blood monocytes and T lymphocytes is differentially suppressed by protein kinase inhibitors.
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Staphylococcal toxic shock syndrome toxin 1-induced tumor necrosis factor alpha and interleukin-1 beta secretion by human peripheral blood monocytes and T lymphocytes is differentially suppressed by protein kinase inhibitors.

机译:蛋白激酶抑制剂可不同程度抑制人外周血单核细胞和T淋巴细胞分泌的葡萄球菌中毒性休克综合征毒素1诱导的肿瘤坏死因子α和白介素1β分泌。

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摘要

The signal transduction pathways by which staphylococcal toxic shock syndrome toxin 1 (TSST-1) induces tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) secretion were examined with various protein kinase inhibitors. TNF-alpha secretion by normal human monocytes and T cells in response to TSST-1 was suppressed by inhibitors of protein kinase C (H7) and tyrosine kinases (genistein). In contrast, the secretion of IL-1 beta was blocked by a cyclic AMP- and cyclic GMP-dependent kinase inhibitor (HA1004) as well as by H7 and genistein. These results suggest that the secretion of TNF-alpha and IL-1 beta may be differentially regulated by TSST-1 and that protein kinases play an important role in mediating cytokine responses to the toxin.
机译:用各种蛋白激酶抑制剂研究了葡萄球菌中毒性休克综合征毒素1(TSST-1)诱导肿瘤坏死因子α(TNF-alpha)和白介素1β(IL-1 beta)分泌的信号转导途径。正常人单核细胞和T细胞对TSST-1的TNF-α分泌受到蛋白激酶C(H7)和酪氨酸激酶(染料木黄酮)抑制剂的抑制。相比之下,IL-1β的分泌被环状AMP和环状GMP依赖性激酶抑制剂(HA1004)以及H7和染料木黄酮所阻断。这些结果表明,TNF-α和IL-1β的分泌可能受到TSST-1的差异调节,并且蛋白激酶在介导对毒素的细胞因子应答中起重要作用。

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