Cytokine-treated human neutrophils contain inducible nitric oxide synthase that produces nitration of ingested bacteria.

• T J Evans

  Department of Infections Diseases and Bacteriology, Royal Postgraduate Medical School, London, United Kingdom. [e-mail]

• L D Buttery

  Department of Infections Diseases and Bacteriology, Royal Postgraduate Medical School, London, United Kingdom. [e-mail]

• A Carpenter

  Department of Infections Diseases and Bacteriology, Royal Postgraduate Medical School, London, United Kingdom. [e-mail]

• D R Springall

  Department of Infections Diseases and Bacteriology, Royal Postgraduate Medical School, London, United Kingdom. [e-mail]

• J M Polak

  Department of Infections Diseases and Bacteriology, Royal Postgraduate Medical School, London, United Kingdom. [e-mail]

• J Cohen

  Department of Infections Diseases and Bacteriology, Royal Postgraduate Medical School, London, United Kingdom. [e-mail]

抄録

Although the production of NO within rodent phagocytes is well-characterized, its production and function within human phagocytes are less clear. We show here that neutrophils within human buffy coat preparations stimulated with a mixture of interleukin 1, tumor necrosis factor alpha, and interferon gamma contain inducible NO synthase mRNA and protein, one of the enzymes responsible for NO production. The protein colocalizes with myeloperoxidase within neutrophil primary granules. Using an inhibitor of NO synthase, L-N-monomethyl arginine, we show that activity of this enzyme is required for the formation of nitrotyrosine around phagocytosed bacteria, most likely through the intermediate production of peroxynitrite, a reaction product of NO and superoxide anions.

収録刊行物

• Proceedings of the National Academy of Sciences

  Proceedings of the National Academy of Sciences 93 (18), 9553-9558, 1996-09-03

  Proceedings of the National Academy of Sciences

キーワード

• Multidisciplinary

詳細情報

• CRID: 1362544419765526784
• NII論文ID: 30016222991
• DOI: 10.1073/pnas.93.18.9553
• ISSN: 10916490
• ISSN: 00278424
• Web Site: https://pnas.org/doi/pdf/10.1073/pnas.93.18.9553
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