Abstract
We determined effects of IL-1α, TNFα and IFNγ on sICAM-1 release in culture media from human aortic smooth muscle cells (AOSMC), dermal microvascular endothelial cells (DMEC), keratinocytes (KC), bronchial epithelial cells (BEC) and lung fibroblasts (LF) as determined by ELISA. Under basal conditions of cultures for 20 h, low concentrations of sICAM-1 were only detected in the culture media of two (DMEC and BEC) of these cell types. IL-1α, TNFα and IFNγ stimulated sICAM-1 from these cells. IFNγ stimulated more shedding from AOSMC, BEC and KC than IL-1α or TNFα. TNFα enhanced more sICAM-1 release from DEMC than from AOSMC, BEC and LF. IL-1α and IFNγ or TNFα and IFNγ 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.
Published Version
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