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血小板、细菌黏附素与肺炎球菌

Platelets, Bacterial Adhesins and the Pneumococcus.

机构信息

Center for Functional Genomics of Microbes, Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, 17489 Greifswald, Germany.

出版信息

Cells. 2022 Mar 25;11(7):1121. doi: 10.3390/cells11071121.

Abstract

Systemic infections with pathogenic or facultative pathogenic bacteria are associated with activation and aggregation of platelets leading to thrombocytopenia and activation of the clotting system. Bacterial proteins leading to platelet activation and aggregation have been identified, and while platelet receptors are recognized, induced signal transduction cascades are still often unknown. In addition to proteinaceous adhesins, pathogenic bacteria such as and also produce toxins such as pneumolysin and alpha-hemolysin. They bind to cellular receptors or form pores, which can result in disturbance of physiological functions of platelets. Here, we discuss the bacteria-platelet interplay in the context of adhesin-receptor interactions and platelet-activating bacterial proteins, with a main emphasis on and . More importantly, we summarize recent findings of how toxins and the pore-forming toxin pneumolysin of interfere with platelet function. Finally, the relevance of platelet dysfunction due to killing by toxins and potential treatment interventions protecting platelets against cell death are summarized.

摘要

全身性感染的致病性或条件致病性细菌与血小板的激活和聚集有关,导致血小板减少和凝血系统的激活。已经鉴定出导致血小板激活和聚集的细菌蛋白,虽然已经识别出血小板受体,但诱导的信号转导级联仍然常常未知。除了蛋白质黏附素外,致病性细菌如 和 也产生毒素,如肺炎球菌溶血素和α-溶血素。它们与细胞受体结合或形成孔,这可能导致血小板的生理功能紊乱。在这里,我们讨论了黏附素-受体相互作用和血小板激活细菌蛋白背景下的细菌-血小板相互作用,主要强调 和 。更重要的是,我们总结了最近的发现,即 毒素和 肺炎球菌溶血素的孔形成毒素如何干扰血小板功能。最后,总结了由于毒素杀伤导致的血小板功能障碍以及保护血小板免受细胞死亡的潜在治疗干预的相关性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1afa/8997422/65026724217f/cells-11-01121-g001.jpg

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