Introduction:
Platelet and fibrin deposits are features of bacterial or endo/exotoxin activation in patients with sepsis and endocarditis. Recent data shows that polysomes in quiescent platelets contain mRNA and other transcripts which provide a mechanism for rapid protein synthesis and a role in inflammation.

Method:
Platelet aggregation, de novo protein synthesis and phosphorylation caused by different bacterial toxins such as Staphylococcus α-toxin and E.coli Lipopolysaccharide (LPS) were tested (in isolation or with different adhesion factors). We employed silver-staining, 2-D western blotting (using antibodies against phosphoserine, phosphothreonine, and phosphotyrosine residues) and mass spectrometric techniques for analysis of the platelet proteome.

Results:
Staphylococcus α-toxin induced platelet aggregation which was dose dependent and was inhibited by Iloprost, and Abciximab. Lipopolysaccharide (LPS) did not affect platelet aggregation.

Collagen, laminin and fibrinogen adherence produced dose and time dependant de novo protein synthesis of bcl-3 and IL-1beta by platelets. This synthesis was further increased by the addition of α-toxin or LPS. In the absence of collagen or fibrinogen exposure, neither α-toxin nor LPS affected platelet protein synthesis. 

Changes in protein synthesis and phosphorylation of a number of other proteins were also seen following LPS or α-toxin stimulation using these adhesion assays. We identified proteins differentially expressed following activation and characterized changes in the proteomic phosphorylation state.

Conclusions:

Bacterial toxins cause profound signal dependant de novo protein synthesis and activation in platelets. These effects are highly dependant upon concomitant adherence of the platelets to collagen and fibrinogen. Such a powerful interaction of toxin and collagen exposure may control platelet activation in disease states like endocarditis. Thus platelets may have previously unrecognized roles in septic and inflammatory conditions including endocarditis.