Therefore, during various viral infections (39, 43), as a result of the formation of platelet/leukocyte aggregates, serotonin secreted from platelets induces immune cells to increase the secretion of antiviral substances

Therefore, during various viral infections (39, 43), as a result of the formation of platelet/leukocyte aggregates, serotonin secreted from platelets induces immune cells to increase the secretion of antiviral substances. ) occurs as a result of activation of vascular endothelium and/or blood leukocytes by platelets, mediated by numerous receptors and (or) numerous plasma substances, in order to activate them towards neutralising effect on bacteria (38, 43, 59). Open in a separate window Physique?1 Effect of inactivating platelets against bacteria (reference in the text). NET, Neutrophil Extracellular Traps; EET, Eosinophil Extracellular Traps; MET, Monocyte-drive Extracellular Traps; PMN, polymorphonuclear cells; MN, mononuclear cells; DC, dendritic cells. In the case of direct neutralisation of bacteria by platelets, with no involvement of plasma substances ( Physique?1 ), these reactions take place between the platelets and bacteria, using their specific receptors, or: – integrin markers GPIb and GPIIb/IIIa (IIb3) – Rabbit Polyclonal to B-RAF TLRs, – match markers (38, 43, 44, 59), – and possibly FcR?IIa, P2Y and CD62P receptors (43, 45, 59). During the direct connection binding of bacteria by platelets mediated by the GPIb and GPIIb/IIIa (IIb3) integrin surface receptors, this reaction was observed during the contamination by (59). In this pathway of direct neutralisation of bacteria by platelets, mediated by TLRs, in the case of bacteria, their lipoteichoic acid is bound by the platelet TLR2 receptor, while in the case of bacteria, their LPS (lipopolysaccharide) is usually bound by the platelet TLR4 marker (8, 20, 31, 44, 59, 95, 111). The direct binding of bacteria by platelets mediated by TLRs is different in humans and mice, because in humans this interaction occurs through the TLR4 receptor, and in mice through the TLR5 and TLR9 markers, and additionally, the bactericidal substances in mice are defensins and microbicidal proteins PMPs (peroxisomal membrane proteins), while in humans, they additionally include -lysine and 4 thymosin (8, 10, 11, 20, 69, 71, 87). However, during this direct pathway of neutralising bacteria by platelets, but with the involvement of plasma substances ( Physique?1 ), this conversation is performed using additionally their specific receptors, which are: – FcR?IIa marker, – GPIIb/IIIa and GPIb integrin marker, – unspecified receptors which bind in a specific sequence to specific plasma substances, that is: – immunoglobulins, – fibrinogen and vWF, and complement components (38, 43, 59), which was found, among others, during the contamination with and and as well as and (29, 59, 87). It is assumed that in the direct way of neutralising bacteria by platelets, or with the involvement of their specific surface receptors, with no involvement of plasma substances and with their involvement, this pathway of (-)-Indolactam V the destructive (-)-Indolactam V effect of platelets on bacteria occurs through ( Physique?1 ): – secretion of biologically active substances – the process of phagocytosis and separately the process of migration, adherence, absorption and intracellular killing – mechanical removal of bacteria – the NET network with the involvement of platelets, cytotoxicity, cytolysis and complement-related bactericidal properties (recommendations in the text). The first pathway of direct neutralisation of bacteria by platelets thanks to the secretion of bactericidal substances contained in their -granules, is usually associated with defensins, microbicidal PMPs, -lysine, thymosin -4 and -5, platelet basic proteins – NAP-2 (CXCL-7), kinocidins, or chemokines with bactericidal activity CXCL4 (PT-4), CCL3 (MIP-2) and CCL5 (RANTES) and IL-8 (CXCL-8), fibrinopeptides A and B, reactive oxygen species (ROS) and connective CTAP-3 (tissue activating peptide 3) (8, 10, 11, 17, 20, 25, 34, 35, 37, 38, 42, 44, 62, 69, 71, 87, 88, 118) as well as cathelicidins and granulysins (119). It has been shown that during contamination with -toxin of sp.,?sp., sp. as (-)-Indolactam V well as and (2, 8, 10, 11, 25, 71), however, the secretion of -defensins by platelets during these infections occurs through the formation of pores, and not through the tubules of platelets (10, 11, 71). Furthermore, bactericidal substances in this direct pathway of platelet.