РОЛЬ ТРОМБОЦИТОВ В ПАТОГЕНЕЗЕ БАКТЕРИАЛЬНЫХ ИНФЕКЦИЙ

In recent years, a critical mass of information has accumulated, which has made it possible to equate platelets to the cells of innate immunity, which ensures the initiation of inflammation and the reactions of innate immunity. In the presented review platelets were examined from the point of view of antibacterial immune reactions. Mechanisms that allow platelets to recognize bacteria and their soluble products as characteristic of immune cells (via TLR2, TLR4, TLR7 and TLR9, FcγRIIa and receptors for complement components), as well as the mechanisms involved in the hemostasis process (GPIb, GPIIb-IIIa). The consequence of the recognition of bacteria is the activation of platelets, the initiation of hemocoagulation and the innate immune response. The ability of platelets to phagocyte bacteriae and stop their growth due to the pronounced microbicidal potential (thrombocidins or microbicidal proteins of platelets and human β-defensins hBD-1, -2 and-3), which these anucleate cells possess, is shown. Discussed that bacteria actively oppose antimicrobial reactions, including using various toxins. Several groups of bacterial toxins have been isolated that activate platelets, destroying the electrochemical gradient of the plasma membrane through membrane perforation. A number of toxins cause the activation of platelets and cells of the immune system, acting as superantigens. In the antibacterial immunity, platelets attract neutrophils, monocytes and activate the complement system. In this case, platelets act together with these cells and proteins, promoting the full disclosure of the microbicidal potential of phagocytes and complement. This is especially important for bacterial infections, which monocytes / macrophages or only platelets cannot control, but, combining, they create the necessary conditions for the clearance of pathogenic bacteria from circulation.

platelets, bacteriae, toxins, inflammation, infective endocarditis, sepsis

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