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首页> 外文期刊>Infection and immunity >Staphylococcal Enterotoxin A Acts through Nitric Oxide Synthase Mechanisms in Human Peripheral Blood Mononuclear Cells To Stimulate Synthesis of Pyrogenic Cytokines
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Staphylococcal Enterotoxin A Acts through Nitric Oxide Synthase Mechanisms in Human Peripheral Blood Mononuclear Cells To Stimulate Synthesis of Pyrogenic Cytokines

机译：葡萄球菌肠毒素A通过人外周血单个核细胞中的一氧化氮合酶机制起作用，以刺激热原细胞因子的合成。

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The pyrogenic response to supernatant fluids obtained from human peripheral blood mononuclear cells (PBMC) stimulated with staphylococcal enterotoxin A (SEA) was characteristic of a response to an endogenous pyrogen in that it was brief and monophasic and was destroyed by heating supernatant fluids at 70°C for 30 min. The febrile responses were in parallel with the levels of interleukin-1 (IL-1), tumor necrosis factor (TNF), interferon-γ (IFN-γ), IL-2, and IL-6 in supernatant fluids obtained from PBMC treated with SEA. Both the pyrogenicity and the levels of IL-1, TNF, IFN-γ, IL-2, and IL-6 in supernatant fluids started to rise at 6 to 18 h and reached their peak levels at 24 to 96 h after SEA incubation. Both the fever and the increased levels of IL-1, TNF, IFN-γ, IL-2, and IL-6 in supernatant fluids obtained from the SEA-stimulated PBMC were decreased by incubating SEA-PBMC with anisomycin (a protein synthesis inhibitor), aminoguanidine (an inhibitor of inducible nitric oxide synthase [NOS]), or dexamethasone (an inhibitor of NOS). The febrile response to supernatant fluids obtained from the SEA-stimulated PBMC was attenuated by adding either anti-IL-1β, anti-TNF-α, or anti-IFN-γ monoclonal antibody (MAb) to supernatant fluids. The antipyretic effects exerted by anti-IL-1β MAb were greater than those exerted by anti-TNF-α or anti-IFN-γ MAb. The data suggest that SEA acts through the NOS mechanisms in PBMC to stimulate synthesis of pyrogenic cytokines (in particular, the IL-1β).
机译：对由葡萄球菌肠毒素A（SEA）刺激的人外周血单核细胞（PBMC）获得的上清液的热原反应是对内源性热原的反应的特征，因为它短暂且单相，并在70°C加热上清液而被破坏C 30分钟。从PBMC处理过的上清液中，发热反应与白细胞介素1（IL-1），肿瘤坏死因子（TNF），干扰素-γ（IFN-γ），IL-2和IL-6的水平平行与SEA。 SEA孵育后，上清液的热原性和IL-1，TNF，IFN-γ，IL-2和IL-6的水平在6至18小时开始上升，并在24至96小时达到峰值。通过将SEA-PBMC与Anisomycin（一种蛋白质合成抑制剂）孵育，可降低发烧和SEA刺激的PBMC上清液中IL-1，TNF，IFN-γ，IL-2和IL-6的水平升高），氨基胍（诱导型一氧化氮合酶[NOS]的抑制剂）或地塞米松（NOS的抑制剂）。通过将抗IL-1β，抗TNF-α或抗IFN-γ单克隆抗体（MAb）添加到上清液中，可以减弱从SEA刺激的PBMC获得的上清液的发热反应。抗IL-1βMAb产生的解热作用大于抗TNF-α或抗IFN-γMAb产生的解热作用。数据表明SEA通过PBMC中的NOS机制起作用，以刺激热原性细胞因子（特别是IL-1β）的合成。

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