Lipid Mediators, Neutrophils, and Endothelial Injury

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Abstract
Neutrophil-mediated endothelial injury may occur in the development of an inflammatory site. The factors contributing to the severity of endothelial injury induced by neutrophils are beginning to be recognized. Close and prolonged contact between neutrophils and the endothelial cell, induced by a variety of mediators, may allow for secretion of toxic products into a limited area and thus overwhelming local defense mechanisms. Similarly, the intensity of neutrophil secretion (proteases or oxygen radicals) once the neutrophil is adherent appears to be of critical importance. In this regard, the ability of bacterial lipopolysaccharides and lipid mediators such as PAF and LTB4 to “prime” the neutrophil for enhanced secretion of oxygen radicals and proteases may be relevant to endothelial injury especially in the complex environment of an inflammatory focus.

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