Figure 1:

Platelet-neutrophil interaction during sepsis. During sepsis, activated platelets attach to neutrophils via a selectin dependent process, namely the release and expression P-selectin of platelet from a-granules which binds to the counter ligand P-selectin glycoprotein ligand (PSGL) expressed on neutophils. Besides that, activated platelet can expression CD40L and then shed it into circulation. Triggering receptor expressed on myeloid cells (TREM)1, triggering receptor expressed on myeloid cells together with CD40L interact with neutrophils which can further promote the activation of neutophils and its generation of reaction oxygen species (ROS). For platelet-expressed CD40L, it can also interact with CD40 on endothelial cells to stimulate the endothelial cell to a pro-inflammatory phenotype: upregulation of intercellular adhesion molecule (ICAM)1 and vascular cell adhesion molecule (VCAM)1, thereby driving neutrophil recruitment. The platelet can also mediate the formation of neutrophil extracellular trap (NET) via the interaction of lymphocyte function-associated antigen (LFA)-1, which can trap free bacteria and enhance the platelet and red blood cell (RBC) adhesion to promote thrombus formation.