Cellular Mechanisms in Airways Inflammation

Part of the series Progress in Inflammation Research pp 223-244

Contribution of endothelial cells to airway inflammation

  • Anne Burke-GaffneyAffiliated withImperial College School of Medicine at the National Heart and Lung Institute, Unit of Critical Care
  • , Paul G. HellewellAffiliated withCardiovascular Research Group, University of Sheffield, Clinical Sciences Centre, Northern General Hospital

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The single layer of endothelial cells that lines the microvessels of the bronchial circulation plays a key role in orchestrating airway inflammation. As a result of their strategic position at the blood-tissue interface, endothelial cells can interact with inflammatory cells and mediators at their luminal and abluminal surface. The response of endothelial cells to an inflammatory stimuli can be broadly divided into vascular and cellular events and this is summarized in Figure 1. The vascular changes include an increase in endothelial permeability of post-capillary venules and vasodilation of arterioles, as a result of the release of, amongst others, endothelial-derived vasodilators. Increased expression of endothelial adhesion molecules and the production of leukocyte chemoattractants from endothelial cells triggers the cellular changes. Together, the vascular and cellular changes culminate in an increase in plasma leakage and leukocyte emigration through the endothelium into the underlying tissue at the site of inflammation.