Abstract
In this study, the role of nitric oxide (NO) on neutrophil migration induced by staphylococcal enterotoxin B (SEB) in the mouse peritoneal cavity was investigated. The NO synthase inhibitors L-NAME and aminoguanidine, as well as dexamethasone, markedly reduced SEB-induced neutrophil influx. In mice with an increased population of peritoneal macrophages, the inhibition of SEB-induced neutrophil influx by these agents was significantly lower. The in vivo treatment with aminoguanidine inhibited only the iNOS activity, whereas L-NAME inhibited both the cNOS and iNOS activities. In conclusion, NO modulates the neutrophil migration in response to SEB through the activity of an iNOS isoform.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology
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Cell Movement / drug effects
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Dexamethasone / pharmacology
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Enterotoxins / toxicity*
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Enzyme Inhibitors / pharmacology
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Guanidines / pharmacology
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Male
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Mice
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NG-Nitroarginine Methyl Ester / pharmacology
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Neutrophil Infiltration / physiology*
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Nitric Oxide / physiology*
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Nitric Oxide Synthase / antagonists & inhibitors
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Nitric Oxide Synthase Type II
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Nitric Oxide Synthase Type III
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Peritoneum / cytology
Substances
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Anti-Inflammatory Agents
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Enterotoxins
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Enzyme Inhibitors
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Guanidines
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Nitric Oxide
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enterotoxin B, staphylococcal
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Dexamethasone
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Nitric Oxide Synthase
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Nitric Oxide Synthase Type II
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Nitric Oxide Synthase Type III
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Nos2 protein, mouse
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Nos3 protein, mouse
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pimagedine
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NG-Nitroarginine Methyl Ester