IL-8 specifically binds to endothelial but not to smooth muscle cells
- PMID: 7868904
IL-8 specifically binds to endothelial but not to smooth muscle cells
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.
Similar articles
-
Neutrophils process interleukin-1beta and interleukin-18 precursors in a caspase-1-like fashion--processing is inhibited by human vascular smooth muscle cells.Eur Cytokine Netw. 2006 Mar;17(1):19-28. Eur Cytokine Netw. 2006. PMID: 16613759
-
Functional and ligand binding specificity of the rabbit neutrophil IL-8 receptor.J Immunol. 1994 Mar 1;152(5):2496-500. J Immunol. 1994. PMID: 8133060
-
IL-3 affects endothelial cell-mediated smooth muscle cell recruitment by increasing TGF beta activity: potential role in tumor vessel stabilization.Oncogene. 2004 Mar 4;23(9):1681-92. doi: 10.1038/sj.onc.1207290. Oncogene. 2004. PMID: 14755254
-
Neutrophil-activating peptides NAP-2 and IL-8 bind to the same sites on neutrophils but interact in different ways. Discrepancies in binding affinities, receptor densities, and biologic effects.J Immunol. 1994 Mar 1;152(5):2467-78. J Immunol. 1994. PMID: 8133058
-
Activation of human basophils through the IL-8 receptor.J Immunol. 1992 Oct 15;149(8):2662-7. J Immunol. 1992. PMID: 1383321
Cited by
-
Role of Herbal Extracts of Catechu from Uncaria gambir in the Treatment of Chronic Diabetic Wounds.Pharmaceuticals (Basel). 2022 Dec 31;16(1):66. doi: 10.3390/ph16010066. Pharmaceuticals (Basel). 2022. PMID: 36678562 Free PMC article.
-
Increased expression of matrix metalloproteinase-1 in systemic vessels of preeclamptic women: a critical mediator of vascular dysfunction.Am J Pathol. 2011 Jan;178(1):451-60. doi: 10.1016/j.ajpath.2010.11.003. Epub 2010 Dec 23. Am J Pathol. 2011. PMID: 21224082 Free PMC article.
-
The cytomegalovirus UL146 gene product vCXCL1 targets both CXCR1 and CXCR2 as an agonist.J Biol Chem. 2010 Mar 19;285(12):9137-46. doi: 10.1074/jbc.M109.002774. Epub 2009 Dec 31. J Biol Chem. 2010. PMID: 20044480 Free PMC article.
-
Neutrophils: key mediators of tumour angiogenesis.Int J Exp Pathol. 2009 Jun;90(3):222-31. doi: 10.1111/j.1365-2613.2009.00641.x. Int J Exp Pathol. 2009. PMID: 19563607 Free PMC article. Review.
-
Mast cell-derived tumour necrosis factor-alpha mediates macrophage inflammatory protein-2-induced recruitment of neutrophils in mice.Br J Pharmacol. 2005 Aug;145(8):1062-8. doi: 10.1038/sj.bjp.0706274. Br J Pharmacol. 2005. PMID: 15937521 Free PMC article.