Abstract
1. Cyclooxygenase-2 (COX-2), along with TNF-α and other proinflammatory cytokines, was hyperinduced in H5N1- infected macrophages in vitro and in epithelial cells of autopsied lung tissues of infected patients. 2. The COX-2 mediated amplification of the proinflammatory response is rapid, and the effects elicited by the H5N1-triggered proinflammatory cascade are broader than those arising from direct viral infection. 3. Selective COX-2 inhibitors suppress the H5N1- hyperinduced cytokines in the proinflammatory cascade.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antiviral Agents / pharmacology*
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Cell Line, Tumor
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Cyclooxygenase 2 / drug effects
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Cyclooxygenase 2 Inhibitors / pharmacology*
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Cytokines / metabolism
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Epithelial Cells / metabolism
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Epithelial Cells / virology
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Humans
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Inflammation / drug therapy
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Inflammation / virology
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Influenza A Virus, H5N1 Subtype / drug effects
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Influenza A Virus, H5N1 Subtype / enzymology*
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Influenza A Virus, H5N1 Subtype / isolation & purification
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Influenza, Human / drug therapy
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Influenza, Human / enzymology*
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Influenza, Human / virology
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Lung / cytology
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Lung / virology
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Macrophages / metabolism
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Macrophages / virology
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Antiviral Agents
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Cyclooxygenase 2 Inhibitors
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Cytokines
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Tumor Necrosis Factor-alpha
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Cyclooxygenase 2