Endothelial cells are key regulators of the inflammatory response. Lining blood vessels, they provide in the steady state an antiinflammatory, anticoagulatory surface. However, in the case of injury or infection, endothelial cells control the adhesion and migration of inflammatory cells, as well as the exchange of fluid from the bloodstream into the damaged tissue. Thus, expression of endothelial adhesion molecules, cytokines, and changes in permeability need to be tightly regulated to allow for a controlled inflammatory response. Acute inflammation is characterized by tissue infiltration of neutrophils, followed by monocytes/macrophages. For successful tissue regeneration and healing, the acute inflammatory response needs to be actively shut down, a process called resolution of inflammation. Unsuccessful resolution may lead to excessive tissue damage and ultimately results in chronic, self-promoting inflammation. This review will summarize recent advances in the field of endothelial biology, which point to an active participation of the endothelial barrier in the resolving process.
Antioxid. Redox Signal. 7, 1744-1754.