Abstract
Apart from their involvement in hemostasis, platelets have been recognized for their contribution to inflammation and defense against microbial agents. The interaction between platelets and bacteria has been well studied in the model of Staphylococcus and Streptococcus but little described in Gram-negative bacteria, especially Escherichia coli. Being involved in the hemolytic uremic syndrome as well as sepsis, it is important to study the mechanisms of interaction between platelets and E. coli. Results of the published studies are heterogeneous. It appears that some strains interact with platelets through the toll-like receptor-4 (TLR-4) and others through the Fc gamma glycoprotein. E. coli mainly uses lipopolysaccharide (LPS) to activate platelets and cause the release of antibacterial molecules, but this is not the case for all strains. In this review, we describe the different mechanisms developed in previous studies, focusing on this heterogeneity of responses that may depend on several factors; mainly, the strain studied, the structure of the LPS and the platelet form used in the studies. We can hypothesize that the structure of O-antigen and an eventual resistance to antibiotics might explain this difference.