TNF and infection: Both cell–cell and cell–matrix adhesions are highly dynamic structures, and extensive remodeling occurs in response to changes in blood flow, as well as permeability-inducing agents released upon infection, inflammation, or wounding, including vascular endothelial growth factor (VEGF), thrombin, histamine, interleukin 1β, interleukin 6, and tumor necrosis factor α (TNF-α).3 In addition, it becomes increasingly apparent that cell–matrix adhesions and cell–cell junctions share a variety of components, and that there is extensive crosstalk between the 2 systems.