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Histamine Inhibits Neutrophil NADPH Oxidase Activity Triggered by the Lipoxin A~4~ Receptor‐Specific Peptide Agonist Trp‐Lys‐Tyr‐Met‐Val‐Met by Å. Betten; C. Dahlgren; S. Hermodsson; K. Hellstrand is a Immunology and Microbiology article available to read on EtoBox.

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## Abstract The vasoactive amine histamine is found at high concentrations in the immune and inflammatory tissues. Earlier studies have revealed that histamine regulates the nicotinamide‐adenine dinucleotide phosphate (NADPH) oxidase‐dependent formation of oxygen radicals by phagocytic cells. However, the effects of histamine on intracellular signal transduction mechanisms of relevance to oxidase regulation remain controversial. For this study, we investigated the effects of histamine on NADPH oxidase activity in human neutrophil granulocytes triggered by a lipoxin A~4~ receptor agonist [the hexapeptide Trp‐Lys‐Tyr‐Met‐Val‐Met (WKYMVM), a formyl peptide receptor (FPR) agonist (the chemotactic tripeptide formylmethionyl‐leucyl‐phenylalanine (fMLF)) and an activator of protein kinase C (phorbol myristate acetate (PMA)]. We report that histamine, acting via H~2~‐type histamine receptors (H~2~R), suppresses NADPH oxidase‐dependent formation of oxygen radicals induced by WKYMVM and fMLF but not that induced by PMA. Peptide‐induced mobilization of granule‐localized complement receptor 3 (CR3) was unaffected by histamine suggesting that the inhibition specifically affected NADPH oxidase a

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Author

Å. Betten; C. Dahlgren; S. Hermodsson; K. Hellstrand

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0300-9475)

Published

2003

Language

EN

Field

Immunology and Microbiology (Life Sciences)