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Am J Physiol Lung Cell Mol Physiol 282: L563-L572, 2002; doi:10.1152/ajplung.00280.2001
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Vol. 282, Issue 3, L563-L572, March 2002

Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection

Ann Marie LeVine1,2, Kevan Hartshorn3, James Elliott1, Jeffrey Whitsett1, and Thomas Korfhagen1

1 Divisions of Pulmonary Biology and 2 Critical Care Medicine, Cincinnati, Ohio 45229-3039; and 3 Department of Medicine and Pathology, Boston University School of Medicine, Boston, Massachusetts 02118

Mice lacking surfactant protein SP-A [SP-A(-/-)] and wild type SP-A(+/+) mice were infected with influenza A virus (IAV) by intranasal instillation. Decreased clearance of IAV was observed in SP-A(-/-) mice and was associated with increased pulmonary inflammation. Treatment of SP-A(-/-) mice with exogenous SP-A enhanced viral clearance and decreased lung inflammation. Uptake of IAV by alveolar macrophages was similar in SP-A(-/-) and SP-A(+/+) mice. Myeloperoxidase activity was reduced in isolated bronchoalveolar lavage neutrophils from SP-A(-/-) mice. B lymphocytes and activated T lymphocytes were increased in the lung and spleen, whereas T helper (Th) 1 responses were increased [interferon-gamma , interleukin (IL)-2, and IgG2a] and Th2 responses were decreased (IL-4, and IL-10, and IgG1) in the lungs of SP-A(-/-) mice 7 days after IAV infection. In the absence of SP-A, impaired viral clearance was associated with increased lung inflammation, decreased neutrophil myeloperoxidase activity, and increased Th1 responses. Because the airway is the usual portal of entry for IAV and other respiratory pathogens, SP-A is likely to play a role in innate defense and adaptive immune responses to IAV.

virus; lung; lectin; surfactant protein-A; surfactant protein-A-deficient mice


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