Surfactant Protein D Enhances Clearance of Influenza A Virus from the Lung In Vivo

• Published in: The Journal of immunology (1950) 2001-11, Vol.167 (10), p.5868-5873
• Main Authors: LeVine, Ann Marie, Whitsett, Jeffrey A, Hartshorn, Kevan L, Crouch, Erika C, Korfhagen, Thomas R
• Format: Article
• Language: English
• Subjects: Animals; Bronchoalveolar Lavage Fluid - immunology; Cytokines - biosynthesis; Glycoproteins - genetics; Glycoproteins - physiology; Influenza A virus; Influenza A virus - isolation & purification; Lung - immunology; Lung - pathology; Lung - virology; Lymphocyte Count; Macrophages, Alveolar - immunology; Mice; Mice, Knockout; Neutrophils - enzymology; Orthomyxoviridae Infections - immunology; Orthomyxoviridae Infections - pathology; Orthomyxoviridae Infections - virology; Peroxidase - metabolism; Phagocytosis; Pulmonary Surfactant-Associated Protein D; Pulmonary Surfactants - genetics; Pulmonary Surfactants - physiology; surfactant protein D; T-Lymphocytes
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.167.10.5868

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.