IL-8 specifically binds to endothelial but not to smooth muscle cells.

U Schönbeck, E Brandt, F Petersen… - … (Baltimore, Md.: 1950 …, 1995 - journals.aai.org
U Schönbeck, E Brandt, F Petersen, HD Flad, H Loppnow
Journal of immunology (Baltimore, Md.: 1950), 1995journals.aai.org
The proinflammatory cytokine and potent chemoattractant IL-8 is involved in regulation of
infectious or inflammatory processes. Human vascular endothelial cells (EC) and smooth
muscle cells (SMC) probably contribute to these responses by recognition and/or production
of rIL-8. We demonstrate here in competitive binding studies with radiolabeled rIL-8 that EC
and fibroblasts, but not SMC, specifically bind IL-8 with low affinity. The binding was not
saturated by ligand concentrations up to 80 nM 125I-rIL-8. Unlabeled neutrophil-activating …
Abstract
The proinflammatory cytokine and potent chemoattractant IL-8 is involved in regulation of infectious or inflammatory processes. Human vascular endothelial cells (EC) and smooth muscle cells (SMC) probably contribute to these responses by recognition and/or production of rIL-8. We demonstrate here in competitive binding studies with radiolabeled rIL-8 that EC and fibroblasts, but not SMC, specifically bind IL-8 with low affinity. The binding was not saturated by ligand concentrations up to 80 nM 125I-rIL-8. Unlabeled neutrophil-activating peptide-2 competed the binding of 125I-rIL-8, although less potently than unlabeled rIL-8, as reported previously for polymorphonuclear neutrophils. In contrast, connective tissue-activating peptide III, platelet factor 4, or lysozyme did not reduce binding of 125I-rIL-8 to EC or fibroblasts. In accordance with these binding studies, EC and fibroblasts, but not SMC, expressed human IL-8 receptor type I mRNA. Neither cell type expressed mRNA for IL-8 receptor type II. Stimulation with IL-1 alpha or LPS did not alter the results obtained in PCR or binding studies. Although SMC did not express specific binding sites for IL-8, Western blot experiments showed that IL-1 alpha-, TNF-, or LPS-stimulated SMC released two major immunoreactive isoforms of IL-8 in a time- and dose-dependent manner. The m.w. were similar to IL-8 isoforms released by EC or mononuclear cells. The differential capacity of EC and SMC to produce IL-8 and express IL-8 binding sites indicates that vascular cell-derived IL-8 may contribute to differential regulation of infectious and inflammatory responses in the vessel wall.
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