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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Inhibition of interleukin-8 production in human endothelial cells by Staphylococcus aureus supernatant.
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Inhibition of interleukin-8 production in human endothelial cells by Staphylococcus aureus supernatant.

机译:金黄色葡萄球菌上清液抑制人内皮细胞中白介素8的产生。

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Recent reports have shown that Staphylococcus aureus infection increases the expression of cytokines and cell adhesion molecules in endothelial cells and enhances leucocyte migration, thereby resulting in bacterial elimination. In this study, we analysed the production of the chemokine interleukin (IL)-8 in human umbilical vein endothelial cells (HUVEC) infected with several S. aureus strains by using reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. We found that the avirulent strains (00-51 and 00-62) increased IL-8 production but the virulent strains (A17 and A151) decreased it at both the mRNA and protein levels. We considered that the inhibition of IL-8 production depended on certain inhibitory factor(s) secreted by bacteria. This was because S. aureus also abolished IL-8 expression in HUVEC treated with cytochalasin D, and the addition of culture supernatants of strains A17 and A151 decreased IL-8 production in HUVEC. This factor(s) in the bacterial culture supernatant inhibited both basal and tumour necrosis factor (TNF)-alpha-induced IL-8 production. In contrast, no inhibitory effect was observed on monocyte chemotactic protein-1 (MCP-1) production. These results indicate that S. aureus can down-regulate IL-8 release in endothelial cells through the secretion of inhibitory factor(s), and this may result in decreased neutrophil recruitment, thus interfering with the host immune response to bacterial infection.
机译:最近的报道表明,金黄色葡萄球菌感染增加了内皮细胞中细胞因子和细胞粘附分子的表达,并增强了白细胞的迁移,从而导致细菌的清除。在这项研究中,我们通过使用逆转录聚合酶链反应和酶联免疫吸附试验,分析了感染了几种金黄色葡萄球菌的人脐静脉内皮细胞(HUVEC)中趋化因子白介素(IL)-8的产生。我们发现无毒力菌株(00-51和00-62)增加了IL-8的产生,而有毒力菌株(A17和A151)在mRNA和蛋白质水平上均降低了IL-8的产生。我们认为IL-8产生的抑制取决于细菌分泌的某些抑制因子。这是因为金黄色葡萄球菌也废除了用细胞松弛素D处理的HUVEC中的IL-8表达,并且菌株A17和A151的培养上清液的添加降低了HUVEC中IL-8的产生。细菌培养上清液中的该因子既抑制基础坏死因子(TNF)-α诱导的IL-8生成,又抑制其生长。相反,未观察到对单核细胞趋化蛋白-1(MCP-1)产生抑制作用。这些结果表明,金黄色葡萄球菌可以通过抑制因子的分泌来下调内皮细胞中IL-8的释放,这可能导致嗜中性粒细胞募集减少,从而干扰宿主对细菌感染的免疫反应。

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