Platelets and the innate immune system: Mechanisms of bacterial-induced platelet activation

It has become clear that platelets are not simply cell fragments that can plug the leak in a damaged blood vessel, they are in fact key components in the innate immune system which is supported by the presence of Toll-like receptors (TLRs) on platelets. As the first responding cell to a site of injury they are well placed to direct the immune response to deal with any resulting exposure to pathogens. The response is triggered by bacteria binding to platelets which usually triggers platelet activation and the secretion of anti-microbial peptides. The main  platelet receptors that mediate these interactions are GPIIb/IIIa, GPIbα, FcνRIIa, complement receptors and TLRs. This may involve direct interactions between bacterial proteins and the receptors or can be mediated by plasma proteins such as fibrinogen, von Willebrand factor, complement and IgG. Here we review the variety of interactions between platelets and bacteria and look at the potential for inhibiting these interactions in diseases such as infective endocarditis and sepsis.