Abstract
In his review of inflammatory responses in infected lungs, Mizgerd (Feb. 14 issue)1 notes that animal models of influenza A virus pneumonia indicate that neither neutrophil leukocytes nor cytokine signaling seems to be important in the case of the highly pathogenic influenza virus infections that cause global pandemics. However, this influenza virus directly inhibits pulmonary epithelial sodium transport, which removes water from the alveolar space by osmosis: Viral hemagglutinin binds to receptors on respiratory epithelial cells, inhibiting epithelial sodium-channel–mediated clearance of pulmonary fluid through a pathway involving phospholipase and protein kinase C.2,3 Reduced epithelial sodium transport also occurs in pulmonary edema associated with septicemia4 and is a potential target for treatment of lung injury by beta-agonists.5

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