Pathogenic events resulting in endovascular disease. Local inflammation activates the binding of fibronectin by ECs through vascular cell adhesion molecules; platelet activation is triggered by cytokines and tissue factor (TF) secreted by monocytes and ECs. Fibronectin also mediates invasion of ECs by S. aureus, allowing for persistence and intracellular growth shielded from host defense. The inflammatory response mediated by T cells and polymorphonuclear neutrophils (PMNs) may be mitigated by the effect of Eap (39, 40). MO, monocyte.