Bacterial–platelet interactions: virulence meets host defense

Abstract

Platelets have historically been viewed as cell fragments that only mediate blood coagulation. Yet, platelets have as – or perhaps even more – important roles in tissue remodeling, modulation of inflammation and antimicrobial host defense. It is evident that platelets interact with prokaryotes directly and indirectly through multiple molecular and cellular mechanisms. The important roles of platelets in antibacterial host defense can be exemplified through contemporary themes in platelet immunobiology. Platelets have unambiguous structures and functions of host defense effector cells. Recent discoveries reveal platelet expression of toll-like and purinonergic receptors, which enable detection and response to bacterial infection, degranulation of an array of microbicidal peptides and coordination of other molecular and celluar host defenses. From multiple perspectives, platelets are now increasingly recognized as critical innate immune effector cells that also bridge and facilitate optimization of adaptive immunity. It follows that clinical deficiencies in platelet quantity or quality are now recognized correlates of increased risk and severity of bacterial and other infections. Along these lines, new evidence suggests that certain prokaryotic organisms may be capable of exploiting platelet interactions to gain a virulence advantage. Indeed, certain bacterial pathogens appear to have evolved highly coordinated means by which to sieze opportunities to bind to surfaces of activated platelets, and exploit them to establish or propagate infection. Hence, it is conceivable that certain bacterial pathogens subvert platelet functions. From these perspectives, the net consequences of bacterial virulence versus platelet host defenses likely decide initial steps towards the ultimate result of infection versus immunity.