Release of soluble ICAM-1 from human lung fibroblasts, aortic smooth muscle cells, dermal microvascular endothelial cells, bronchial epithelial cells, and keratinocytes

We determined effects of IL-1 alpha, TNF alpha and IFN gamma on sICAM-1 rel ease in culture media from human aortic smooth muscle cells (AOSMC), dermal microvascular endothelial cells (DMEC), keratinocytes (KC), bronchial epit helial cells (BEC) and lung fibroblasts (LF) as determined by ELISA. Under basal conditions of cultures for 20 h, low concentrations of sICAM-1 were o nly detected in the culture media of two (DMEC and BEC) of these cell types . IL-1 alpha, TNF alpha and IFN gamma stimulated sICAM-1 from these cells. IFN gamma stimulated more shedding from AOSMC, BEC and KC than IL-1 alpha o r TNF alpha. TNF alpha enhanced more sICAM-1 release from DEMC than from AO SMC, BEC and LF, IL-1 alpha and IFN gamma or TNF alpha and IFN gamma acted synergistically to enhance shedding of sICAM-1 from these cells, The levels sICAM-1 in pathophysiological conditions may influence leukocyte-vascular cell interactions to block leukocyte transmigration to tissue injury sites as a negative feedback mechanism. (C) 1999 Academic Press.