Regulation of inflammatory vascular damage.

The acute inflammatory response is comprised of an elaborate cascade of mediators that control an ordered sequence of events resulting in the recruitment of neutrophils to the site of infection or injury. Microvascular injury occurring during acute inflammation often results in increased vascular permeability and microvascular haemorrhage. Damage to vascular endothelial cells, basement membrane, and matrix components results from both neutrophil-dependent and neutrophil-independent mechanisms and is also dependent on the organ/tissue source of the endothelial cells. Neutrophil-mediated injury of endothelial cells involves a complex cascade in which products from both cell types affect the cytotoxic outcome. It is also clear that the acute inflammatory response is carefully regulated by the endogenous gene expression of both pro-inflammatory and anti-inflammatory mediators. Control of acute inflammation seems to relate to activation of the transcription factor NFkappaB. To appreciate the interrelationship between multiple contributing factors of inflammatory vascular injury, one must first have an understanding of the inflammatory mediator cascades which bring about the recruitment of neutrophils to the site of inflammation. In this review it is discussed how inflammatory mediators, as well as the products of activated neutrophils, affect the outcome of the acute inflammatory response. Copyright 2000 John Wiley & Sons, Ltd.