Figure 1.

Platelets-neutrophil interactions and NETs. (A) Key adhesion molecules involved in platelet-neutrophil interactions. These interactions not only provide mechanisms of cell attachment but may also trigger intracellular signaling, promoting cell activation, resulting in the upregulation of additional adhesion and effector molecules. Effector molecules from both cells, such as cathepsin G from neutrophils, in turn modulate neutrophil-platelet physical interactions through cleavage of PSGL-1 and GPIb. (B) Effect of NET inhibition (PAD4^−/− mice) or disruption (DNase treatment) in animal models of (Bi) endocarditis (18), (Bii) bacterial sepsis (19), and (Biii) bacterial pneumonia (20). Overall, targeting NETs is associated with reduced inflammation and organ damage; however, this effect has been shown to favor bacterial dissemination.