Abstract
Kinin B1 receptors are induced by various inflammatory mediators. The aim of the present study was to investigate the effect of the CXC chemokine IL-8 on kinin B1 receptor expression in IMR-90 cells, by performing binding studies and Northern blot analysis of B1 receptor mRNA levels. We demonstrated here that the density of the kinin B1 receptors could be increased by the chemokine IL-8 in a concentration- and time-dependent manner. IL-8 also increased the kinin B1 receptor mRNA level in IMR-90 cells. IL-8-induced B1 receptor expression could be totally abolished by pretreatment with the metabolic inhibitors. Furthermore, expression was markedly reduced by antibodies to human IL-1alpha. In conclusion, IL-8 increased the expression of kinin B1 receptors in IMR-90 cells and this effect is likely to be secondary to the production of IL-1beta.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antibodies / pharmacology
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Antigens, CD / biosynthesis
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Antigens, CD / genetics
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Cell Line
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Fibroblasts / cytology
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Fibroblasts / drug effects
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Humans
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Interleukin-1 / immunology
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Interleukin-8 / immunology
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Interleukin-8 / pharmacology*
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Kallidin / analogs & derivatives
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Kallidin / metabolism
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Lung / cytology
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Lung / drug effects*
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Lung / embryology
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Protein Binding
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RNA, Messenger / analysis
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Receptor, Bradykinin B1
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Receptors, Bradykinin / biosynthesis*
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Receptors, Bradykinin / genetics
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Receptors, Interleukin / biosynthesis
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Receptors, Interleukin / genetics
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Receptors, Interleukin-8A
Substances
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Antibodies
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Antigens, CD
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Interleukin-1
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Interleukin-8
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RNA, Messenger
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Receptor, Bradykinin B1
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Receptors, Bradykinin
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Receptors, Interleukin
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Receptors, Interleukin-8A
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bradykinin, Lys-Leu(8)-desArg(9)-
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Kallidin