Abstract
Chlorinated amines are long-lived oxidants released from inflammatory cells. They have been observed to alter the function of important inflammatory molecules. Whether they can contribute directly to the inflammatory alteration of cellular barriers is not known. Monolayers of cultured porcine pulmonary artery endothelial cells, monolayers of cultured dog kidney tubular epithelial cells (MDCK), and the vascular surface of an isolated perfused rabbit lung were exposed to taurine chloramine. Taurine chloramine increased albumin flux across the endothelium, decreased the electrical resistance across the epithelium, and increased the hydraulic conductivity of the rabbit lung vasculature. These alterations in barrier function appeared to occur in the absence of cytolysis of the cells making up the barriers. These results suggest that chlorinated amines, long-lived oxidants released from inflammatory cells, may contribute directly to alteration of cellular barriers.
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