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首页> 外文期刊>Infection and immunity >Staphylococcal Enterotoxin B Primes Cytokine Secretion and Lytic Activity in Response to Native Bacterial Antigens
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Staphylococcal Enterotoxin B Primes Cytokine Secretion and Lytic Activity in Response to Native Bacterial Antigens

机译：葡萄球菌肠毒素B引发细胞因子的分泌和对自然细菌抗原的裂解活性。

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Superantigens stimulate T-lymphocyte proliferation and cytokine production, but the effects of superantigen exposure on cell function within a complex, highly regulated immune response remain to be determined. In this study, we demonstrate that superantigen exposure significantly alters the murine host response to bacterial antigens in an in vitro coculture system. Two days after exposure to the superantigen staphylococcal enterotoxin B, splenocytes cultured withStreptococcus mutans produced significantly greater amounts of gamma interferon (IFN-γ) and interleukin-12 than did sham-injected controls. The majority of IFN-γ production appeared to be CD8+ T-cell derived since depletion of this cell type dramatically reduced the levels of IFN-γ. To study host cell damage that may occur following superantigen exposure, we analyzed cytotoxicity to “bystander” fibroblast cells cultured with splenocytes in the presence of bacterial antigens. Prior host exposure to staphylococcal enterotoxin B significantly enhanced fibroblast cytotoxicity in the presence of bacteria. Neutralization of IFN-γ decreased the amount of cytotoxicity observed. However, a greater reduction was evident when splenocyte-bacterium cocultures were separated from the bystander cell monolayer via a permeable membrane support. Increased cytotoxicity appears to be primarily dependent upon cell-cell contact. Collectively, these data indicate that overproduction of inflammatory cytokines may alter the activity of cytotoxic immune cells. Superantigen exposure exacerbates cytokine production and lytic cell activity when immune cells encounter bacteria in vitro and comparable activities could possibly occur in vivo.
机译：超抗原刺激T淋巴细胞的增殖和细胞因子的产生，但是超抗原暴露对复杂，高度调节的免疫反应中细胞功能的影响尚待确定。在这项研究中，我们证明了超抗原暴露在体外共培养系统中显着改变了鼠宿主对细菌抗原的反应。暴露于超抗原葡萄球菌肠毒素B后两天，与变形链球菌相比，用变形链球菌培养的脾细胞产生的γ-干扰素（IFN-γ）和白介素12的量明显大于假注射的对照。大部分IFN-γ产生似乎是CD8 + T细胞衍生的，因为这种细胞类型的耗竭极大地降低了IFN-γ的水平。为了研究超抗原暴露后可能发生的宿主细胞损伤，我们分析了在细菌抗原存在下用脾细胞培养的“旁观者”成纤维细胞的细胞毒性。在细菌存在下，先前宿主暴露于葡萄球菌肠毒素B会显着增强成纤维细胞的细胞毒性。 IFN-γ的中和降低了观察到的细胞毒性。但是，当脾细胞-细菌共培养物通过可渗透膜支持物与旁观者细胞单层分离时，明显减少。细胞毒性的增加似乎主要取决于细胞与细胞的接触。总的来说，这些数据表明炎性细胞因子的过量产生可能改变细胞毒性免疫细胞的活性。当免疫细胞在体外遇到细菌时，超抗原的暴露会加剧细胞因子的产生和裂解细胞的活性，体内可能发生相当的活性。

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