Neutrophil-derived OSM triggers endothelial gp130 signaling that enhances P-selectin–dependent leukocyte adhesion and thrombosis. Neutrophils rolling on P-selectin release OSM (A) that triggers gp130 signaling in endothelial cells (B). Signaling through gp130 augments clustering of P-selectin in clathrin-coated pits, which enhances rolling of neutrophils and monocytes and facilitates integrin-dependent arrest (B-C). In flow-restricted veins, the increased leukocyte adhesion promotes thrombosis (D). See “Discussion” for details.