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Toll 样受体 2 和脂蛋白样脂蛋白增强金黄色葡萄球菌对上皮细胞的侵袭。

Toll-Like Receptor 2 and Lipoprotein-Like Lipoproteins Enhance Staphylococcus aureus Invasion in Epithelial Cells.

机构信息

Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine (IMIT), University of Tübingen, Tübingen, Germany.

Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine (IMIT), University of Tübingen, Tübingen, Germany

出版信息

Infect Immun. 2018 Jul 23;86(8). doi: 10.1128/IAI.00343-18. Print 2018 Aug.

Abstract

contains a certain subclass of lipoproteins, the so-called lipoprotein-like lipoproteins (Lpl's), that not only represent Toll-like receptor 2 (TLR2) ligands but are also involved in host cell invasion. Here we addressed the question of which factors contribute to Lpl-mediated invasion of epithelial cells and keratinocytes. For this purpose, we compared the invasiveness of USA300 and its Δ mutant under different conditions. In the presence of the matrix proteins IgG, fibrinogen (Fg), and fibronectin (Fn), and of fetal bovine serum (FBS), the invasion ratio was increased in both strains, and always more in USA300 than in its Δ mutant. Interestingly, when we compared the invasion of HEK-0 and HEK-TLR2 cells, the cells expressing TLR2 showed a 9-times-higher invasion frequency. When HEK-TLR2 cells were additionally stimulated with a synthetic lipopeptide, PamCSK (P3C), the invasion frequency was further increased. A potential reason for the positive effect of TLR2 on invasion could be that TLR2 activation by P3C also activates F-actin formation. Here we show that invasion depends on a number of factors, on the host side as well as on the bacterial side.

摘要

包含特定亚类的脂蛋白,即所谓的脂蛋白样脂蛋白(Lpl),不仅代表 Toll 样受体 2(TLR2)配体,而且还参与宿主细胞入侵。在这里,我们探讨了哪些因素有助于 Lpl 介导的上皮细胞和角质形成细胞的入侵。为此,我们比较了 USA300 及其 Δ突变体在不同条件下的侵袭性。在存在基质蛋白 IgG、纤维蛋白原(Fg)和纤维连接蛋白(Fn)以及胎牛血清(FBS)的情况下,两种菌株的侵袭率均增加,且 USA300 中的侵袭率总是高于其 Δ突变体。有趣的是,当我们比较 HEK-0 和 HEK-TLR2 细胞的侵袭时,表达 TLR2 的细胞显示出 9 倍更高的侵袭频率。当用合成脂肽 PamCSK(P3C)进一步刺激 HEK-TLR2 细胞时,侵袭频率进一步增加。TLR2 对侵袭的积极影响的一个潜在原因可能是 P3C 激活 TLR2 也激活了 F-肌动蛋白的形成。在这里,我们表明 侵袭取决于许多因素,包括宿主侧和细菌侧。

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