Yadav Vivek K, Singh Pradeep K, Agarwal Vishnu, Singh Sunil K
Department of Biotechnology Motilal Nehru National Institute of Technology Allahabad, Prayagraj, India.
Department of Animal Sciences, Central University of Punjab, Bathinda, Punjab, India.
Curr Pharm Des. 2019;25(38):4041-4052. doi: 10.2174/1381612825666190925163347.
Platelets are typically recognized for their roles in the maintenance of hemostasis and vascular wall repair to reduce blood loss. Beyond hemostasis, platelets also play a critical role in pathophysiological conditions like atherosclerosis, stroke, thrombosis, and infections. During infection, platelets interact directly and indirectly with bacteria through a wide range of cellular and molecular mechanisms. Platelet surface receptors such as GPIbα, FcγRIIA, GPIIbIIIa, and TLRs, etc. facilitate direct interaction with bacterial cells. Besides, the indirect interaction between platelet and bacteria involves host plasma proteins such as von Willebrand Factor (vWF), fibronectin, IgG, and fibrinogen. Bacterial cells induce platelet activation, aggregation, and thrombus formation in the microvasculature. The activated platelets induce the Neutrophil Extracellular Traps (NETs) formation, which further contribute to thrombosis. Thus, platelets are extensively anticipated as vital immune modulator cells during infection, which may further lead to cardiovascular complications. In this review, we cover the interaction mechanisms between platelets and bacteria that may lead to the development of thrombotic disorders. Platelet receptors and other host molecules involved in such interactions can be used to develop new therapeutic strategies to combat against infection-induced cardiovascular complications. In addition, we highlight other receptor and enzyme targets that may further reduce infection-induced platelet activation and various pathological conditions.
血小板通常因其在维持止血和血管壁修复以减少失血方面的作用而被认可。除了止血作用外，血小板在动脉粥样硬化、中风、血栓形成和感染等病理生理状况中也起着关键作用。在感染期间，血小板通过多种细胞和分子机制直接和间接地与细菌相互作用。血小板表面受体如糖蛋白Ibα（GPIbα）、FcγRIIA、糖蛋白IIbIIIa（GPIIbIIIa）和Toll样受体（TLRs）等促进与细菌细胞的直接相互作用。此外，血小板与细菌之间的间接相互作用涉及宿主血浆蛋白，如血管性血友病因子（vWF）、纤连蛋白、免疫球蛋白G（IgG）和纤维蛋白原。细菌细胞在微血管中诱导血小板活化、聚集和血栓形成。活化的血小板诱导中性粒细胞胞外陷阱（NETs）形成，这进一步促进血栓形成。因此，血小板被广泛认为是感染期间重要的免疫调节细胞，这可能进一步导致心血管并发症。在本综述中，我们涵盖了血小板与细菌之间可能导致血栓性疾病发生的相互作用机制。参与此类相互作用的血小板受体和其他宿主分子可用于开发新的治疗策略，以对抗感染引起的心血管并发症。此外，我们强调了其他可能进一步减少感染诱导的血小板活化和各种病理状况的受体和酶靶点。
