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首页> 外文期刊>The journal of microbiology >Involvement of phosphatidylinositol 3-Kinase/Akt signaling pathway in β1 integrin-mediated internalization of Staphylococcus aureus by alveolar epithelial cells
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Involvement of phosphatidylinositol 3-Kinase/Akt signaling pathway in β1 integrin-mediated internalization of Staphylococcus aureus by alveolar epithelial cells

机译:肺泡上皮细胞参与磷脂酰肌醇3-激酶/ Akt信号通路参与β1整合素介导的金黄色葡萄球菌内在化

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摘要

The invasion of Staphylococcus aureus into alveolar epithelial cells is regarded as the key step for S. aureus lung infection. However, the mechanism of internalization of S. aureus by alveolar epithelial cells is not clear, and was the aim of this investigation Human lung adenocarcinomic epithelial cells and A549 cells were used. Human β1 integrin and rat β1 integrin were detected by real-time reverse transcription (RT)-PCR. The expressions of β1 integrin, Akt and p-Akt were detected by Western blot analysis. To further investigate the role of β1 integrin in S. aureus internalization by alveolar epithelial cells, we next performed siRNA-mediated knockdown of β1 integrin expression. In this study, we found that S. aureus invades human alveolar epithelial cells and rat primary alveolar epithelial cells. The β1 integrin ligand competitive inhibitor, GRGDS-peptide, blocked the internalization of S. aureus by A549 cells. Knockdown of β1 integrin also inhibited the internalization of S. aureus. In addition, the PI3K/Akt signaling pathway in alveolar epithelial cells was activated by the infection with S. aureus. Furthermore, Akt phosphorylation was abolished by transient transfection with β1 integrin siRNA in A549 cells challenged with S. aureus. Our results suggest that the phosphatidylinositol 3-kinase/Akt signaling pathway plays an important role in β1 integrin-mediated internalization of S. aureus by alveolar epithelial cells.
机译:金黄色葡萄球菌侵入肺泡上皮细胞被认为是金黄色葡萄球菌肺部感染的关键步骤。但是,肺泡上皮细胞对金黄色葡萄球菌内在化的机制尚不清楚,这是本研究的目的。使用了人肺腺癌上皮细胞和A549细胞。通过实时逆转录(RT)-PCR检测人β1整合素和大鼠β1整合素。 Western blot法检测β1整合素,Akt和p-Akt的表达。为了进一步研究β1整合素在肺泡上皮细胞对金黄色葡萄球菌内在化中的作用,我们接下来进行了siRNA介导的β1整合素表达的敲低。在这项研究中,我们发现金黄色葡萄球菌侵入人的肺泡上皮细胞和大鼠原发性肺泡上皮细胞。 β1整联蛋白配体竞争性抑制剂GRGDS肽阻断了A549细胞对金黄色葡萄球菌的内在化。 β1整合素的抑制还抑制金黄色葡萄球菌的内在化。此外,金黄色葡萄球菌感染激活了肺泡上皮细胞中的PI3K / Akt信号通路。此外,通过在金黄色葡萄球菌攻击的A549细胞中用β1整合素siRNA瞬时转染消除了Akt磷酸化。我们的结果表明,磷脂酰肌醇3-激酶/ Akt信号通路在肺泡上皮细胞的β1整合素介导的金黄色葡萄球菌内化中起重要作用。

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