Staphylococcal Adhesion and Host Cell Invasion: Fibronectin-Binding and Other Mechanisms.
Staphylococcal Adhesion and Host Cell Invasion: Fibronectin-Binding and Other Mechanisms.
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DOI：
10.3389/fmicb.2017.02433
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发表时间：
2017
影响因子：
5.2
通讯作者：
Diot A
中科院分区：
文献类型：
--
作者：
Josse J;Laurent F;Diot A
来自葡萄球菌属的寄生菌可引起危及生命的感染，如肺炎、心内膜炎、骨和关节感染以及败血症。这种致病性与它们直接结合细胞外基质或宿主细胞的能力密切相关。粘附确实是生物膜形成或宿主细胞入侵的第一步，其保护细菌免受宿主免疫系统的侵害并促进慢性感染。粘附依赖于称为粘附素的表面蛋白的库的表达，特别是识别粘附基质分子的微生物表面组分。在这篇简短的综述中，我们讨论了金黄色葡萄球菌粘附并侵入非专职吞噬细胞的主要途径（FnBP-Fn-α5β1整联蛋白）以及替代途径。然后，我们研究凝固酶阴性葡萄球菌的相应机制。目前对导致内化的分子机制了解甚少。因此，填补文献中的这一空白将是限制临床实践中葡萄球菌感染持续时间的重要一步。
Opportunistic bacteria from the genus Staphylococcus can cause life-threatening infections such as pneumonia, endocarditis, bone and joint infections, and sepsis. This pathogenicity is closely related to their capacity to bind directly to the extracellular matrix or to host cells. Adhesion is indeed the first step in the formation of biofilm or the invasion of host cells, which protect the bacteria from the host immune system and facilitate chronic infection. Adhesion relies on the expression of a repertoire of surface proteins called adhesins, notably microbial surface components recognizing adhesive matrix molecules. In this short review, we discuss the main pathway (FnBP-Fn-α5β1 integrin), as well as alternatives, through which Staphylococcus aureus adheres to and then invades non-professional phagocytic cells. We then examine the corresponding mechanisms for coagulase negative staphylococci. There is currently a little understanding of the molecular mechanisms that lead to internalization. Filling this gap in the literature would therefore be an important step toward limiting the duration of staphylococci infections in clinical practice.
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