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首页> 外文期刊>Infection and immunity >Abelson Tyrosine Kinase Facilitates Salmonella enterica Serovar Typhimurium Entry into Epithelial Cells
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Abelson Tyrosine Kinase Facilitates Salmonella enterica Serovar Typhimurium Entry into Epithelial Cells

机译：Abelson酪氨酸激酶有助于肠炎沙门氏菌血清鼠伤寒沙门氏菌进入上皮细胞

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The intracellular gram-negative bacterial pathogen Salmonella enterica serovar Typhimurium gains entry into nonphagocytic cells by manipulating the assembly of the host actin cytoskeleton. S. enterica serovar Typhimurium entry requires a functional type III secretion system, a conduit through which bacterial effector proteins are directly translocated into the host cytosol. We and others have previously reported the enhancement of tyrosine kinase activities during Salmonella serovar Typhimurium infection; however, neither specific kinases nor their targets have been well characterized. In this study, we investigated the roles of the cellular Abelson tyrosine kinase (c-Abl) and the related protein Arg in the context of serovar Typhimurium infection. We found that bacterial internalization was inhibited by more than 70% in cells lacking both c-Abl and Arg and that treatment of wild-type cells with a pharmaceutical inhibitor of the c-Abl kinase, STI571 (imatinib), reduced serovar Typhimurium invasion efficiency to a similar extent. Bacterial infection led to enhanced phosphorylation of two previously identified c-Abl substrates, the adaptor protein CT10 regulator of kinase (CrkII) and the Abelson-interacting protein Abi1, a component of the WAVE2 complex. Furthermore, overexpression of the nonphosphorylatable form of CrkII resulted in decreased invasion. Taken together, these findings indicate that c-Abl is activated during S. enterica serovar Typhimurium infection and that its phosphorylation of multiple downstream targets is functionally important in bacterial internalization.
机译：细胞内革兰氏阴性细菌病原体沙门氏菌血清鼠伤寒通过操纵宿主肌动蛋白细胞骨架的组装进入非吞噬细胞。 S。肠伤寒鼠伤寒沙门氏菌的进入需要功能性的III型分泌系统，即细菌效应蛋白直接通过该管道转运到宿主细胞质中的管道。我们和其他人先前已经报道了沙门氏菌血清鼠伤寒感染过程中酪氨酸激酶活性的增强。但是，特异性激酶及其靶标均未得到很好的表征。在这项研究中，我们调查了细胞Abelson酪氨酸激酶（c-Abl）和相关蛋白Arg在血清型鼠伤寒感染中的作用。我们发现，在缺乏c-Abl和Arg的细胞中，细菌内在化受到了超过70％的抑制，并且用c-Abl激酶STI571（伊​​马替尼）的药物抑制剂处理野生型细胞降低了血清型鼠伤寒侵袭效率在相似的程度上。细菌感染导致两个先前鉴定的c-Abl底物，激酶的衔接蛋白CT10调节剂（CrkII）和与Abelson相互作用的蛋白Abi1（WAVE2复合物的一个组成部分）的磷酸化增强。此外，CrkII的非磷酸化形式的过表达导致侵袭减少。综上，这些发现表明c-Abl在 S期间被激活。肠杆菌血清型鼠伤寒感染及其在多个下游靶点的磷酸化在细菌内在化方面具有重要作用。

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