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Divisions of
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Pulmonary Biology and
Critical Care Medicine, Children’s Hospital Medical Center, Cincinnati, OH 45229;
Department of Medicine and Pathology, Boston University School of Medicine, Boston, MA 02118; and
Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110
Mice lacking surfactant protein surfactant protein D (SP-D-/-) and wild-type mice (SP-D+/+) were infected with influenza A virus (IAV) by intranasal instillation. IAV infection increased the endogenous SP-D concentration in wild-type mice. SP-D-deficient mice showed decreased viral clearance of the Phil/82 strain of IAV and increased production of inflammatory cytokines in response to viral challenge. However, the less glycosylated strain of IAV, Mem/71, which is relatively resistant to SP-D in vitro, was cleared efficiently from the lungs of SP-D-/- mice. Viral clearance of the Phil/82 strain of IAV and the cytokine response were both normalized by the coadministration of recombinant SP-D. Since the airway is the usual portal of entry for influenza A virus and other respiratory pathogens, SP-D is likely to play an important role in innate defense responses to IAV.
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 J. Akiyama, A. Hoffman, C. Brown, L. Allen, J. Edmondson, F. Poulain, and S. Hawgood Tissue Distribution of Surfactant Proteins A and D in the Mouse J. Histochem. Cytochem., July 1, 2002; 50(7): 993 - 996. [Abstract] [Full Text] [PDF]
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M. T. Stahlman, M. E. Gray, W. M. Hull, and J. A. Whitsett Immunolocalization of Surfactant Protein-D (SP-D) in Human Fetal, Newborn, and Adult Tissues J. Histochem. Cytochem., May 1, 2002; 50(5): 651 - 660. [Abstract] [Full Text] [PDF]
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A. M. LeVine, K. Hartshorn, J. Elliott, J. Whitsett, and T. Korfhagen Absence of SP-A modulates innate and adaptive defense responses to pulmonary influenza infection Am J Physiol Lung Cell Mol Physiol, March 1, 2002; 282(3): L563 - L572. [Abstract] [Full Text] [PDF]
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