Abstract
Interleukin-8 (IL-8) is implicated in the pathogenesis of a large number of neutrophil-driven inflammatory diseases. Although the cytokine activates neutrophils through a receptor, no information is available regarding the regulation of IL-8 receptor (IL-8R) expression. The present study shows that, compared to control, the bacterial products--formylpeptide and LPS (serum-activated) upregulate IL-8 receptor by 54% and 115%, respectively, the former by degranulation of the secretory vesicle and the latter by de novo protein synthesis. The newly expressed IL-8R could be demonstrated with anti-IL-8R-antibody and by autoradiogram of the receptor crosslinked with [125I]IL-8. The study may be useful for understanding the potential role of IL-8 during neutrophil mediated inflammatory response.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antibodies / immunology
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Antigens, CD / immunology
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Antigens, Differentiation, Myelomonocytic / immunology
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Cross-Linking Reagents
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Humans
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Interleukin-8 / metabolism
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Lipopolysaccharide Receptors
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Lipopolysaccharides / pharmacology*
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N-Formylmethionine Leucyl-Phenylalanine / pharmacology*
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Neutrophil Activation
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Neutrophils / drug effects
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Neutrophils / metabolism*
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Polymyxin B / pharmacology
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Receptors, Interleukin / immunology
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Receptors, Interleukin / metabolism*
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Receptors, Interleukin-8A
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Recombinant Proteins / metabolism
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Up-Regulation
Substances
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Antibodies
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Antigens, CD
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Antigens, Differentiation, Myelomonocytic
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Cross-Linking Reagents
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Interleukin-8
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Lipopolysaccharide Receptors
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Lipopolysaccharides
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Receptors, Interleukin
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Receptors, Interleukin-8A
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Recombinant Proteins
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N-Formylmethionine Leucyl-Phenylalanine
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Polymyxin B