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首页> 外文期刊>The FEBS journal >Staphylococcal enterotoxin C1-induced pyrogenic cytokine production in human peripheral blood mononuclear cells is mediated by NADPH oxidase and nuclear factor-kappa B
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Staphylococcal enterotoxin C1-induced pyrogenic cytokine production in human peripheral blood mononuclear cells is mediated by NADPH oxidase and nuclear factor-kappa B

机译：NADPH氧化酶和核因子-κB介导人外周血单核细胞中葡萄球菌肠毒素C1诱导的热原细胞因子的产生

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摘要

The staphylococcal enterotoxins produced by Staphylococcus aureus are associated with pyrogenic response in humans and primates. This study investigates the role of NADPH oxidase and nuclear factor-kappa B (NF-kappaB) on enterotoxin staphylococcal enterotoxin C1 (SEC1)-induced pyrogenic cytokine production in human peripheral blood mononuclear cells (PBMC). The results indicate that the febrile response to the supernatant fluids of SEC1-stimulated PBMC in rabbits was in parallel with the levels of interleukin-1beta and interleukin-6 in the supernatants. The release of interleukin-1beta and interleukin-6, nuclear translocation of NF-kappaB and its DNA binding activity in the SEC1-stimulated PBMC were time-dependent and were completely eliminated by pyrrolidine dithiocarbamate or SN-50 (NF-kappaB inhibitors). The release of reactive oxygen species in the supernatants and translocation of the NADPH oxidase p47(phox) subunit to the plasma membrane of SEC1-stimulated PBMC were time-dependent. Administration of apocynin (NADPH oxidase inhibitor) attenuated the febrile response to the supernatants in rabbits and decreased the translocation of NADPH oxidase p47(phox) subunit and NF-kappaB activity in the SEC1-stimulated PBMC, and suppressed reactive oxygen species and pyrogenic cytokine production in the supernatants. Taken together, SEC1 may act through an NADPH oxidase mechanism to release reactive oxygen species, which activate NF-kappaB in PBMC to stimulate the synthesis of pyrogenic cytokines that trigger a fever response in rabbits.
机译：金黄色葡萄球菌产生的葡萄球菌肠毒素与人类和灵长类动物的热原反应有关。这项研究调查了NADPH氧化酶和核因子-κB（NF-kappaB）在人外周血单核细胞（PBMC）中由肠毒素葡萄球菌肠毒素C1（SEC1）诱导的热原细胞因子产生中的作用。结果表明，对SEC1刺激的PBMC上清液的发热反应与上清液中白介素-1β和白介素-6的水平平行。在SEC1刺激的PBMC中，白介素1β和白介素6的释放，NF-κB的核易位及其DNA结合活性是时间依赖性的，并被吡咯烷二硫代氨基甲酸酯或SN-50（NF-κB抑制剂）完全消除。上清液中活性氧的释放以及NADPH氧化酶p47（phox）亚基向SEC1刺激的PBMC质膜的迁移是时间依赖性的。 Apocynin（NADPH氧化酶抑制剂）的给药减弱了兔对上清液的发热反应，并降低了SEC1刺激的PBMC中NADPH氧化酶p47（phox）亚基的易位和NF-κB的活性，并抑制了活性氧和热原性细胞因子的产生在上清液中。综上所述，SEC1可能通过NADPH氧化酶机制释放活性氧，从而激活PBMC中的NF-κB，从而刺激引起兔发烧反应的热原性细胞因子的合成。

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