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Published ahead of print on March 11, 2004, doi:10.1165/rcmb.2003-0107OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 2, August 2004, 193-199

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Submitted on March 26, 2003
Revised on March 11, 2004

SURFACTANT PROTEIN-D ENHANCES PHAGOCYTOSIS AND PULMONARY CLEARANCE OF RESPIRATORY SYNCYTIAL VIRUS

Ann Marie LeVine1*, James Elliott2, Jeffrey Whitsett2, Anon Srikiatkhachorn3, Erika Crouch4, Nihal DeSilva4, and Thomas Korfhagen2

1 Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Divisions of Pulmonary Biology and Critical Care Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA, 2 Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA, 3 Department of Pulmonary Medicine, Allergy and Clinical Immunology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA, 4 Department of Pathology, Washington University School of Medicine, St. Louis, MO, USA

* To whom correspondence should be addressed. E-mail: annmarie.levine{at}cchmc.org.

Surfactant protein D gene targeted (SP-D -/-) and wild type mice were infected with respiratory syncytial virus (RSV) by intratracheal instillation. Decreased clearance of RSV was observed in SP-D -/- mice. Deficiency of SP-D was associated with increased inflammation and inflammatory cell recruitment in the lung after infection. In vitro, SP-D bound RSV infected Vero cells. Binding was inhibited with EDTA and maltose suggesting the carbohydrate recognition domain of SP-D recognizes RSV glycoproteins in a calcium dependent manner. SP-D bound specifically to the RSV proteins G and F. Phagocytosis of RSV by alveolar macrophages was reduced in the absence of SP-D in vivo and SP-D enhanced phagocytosis of RSV by alveolar macrophages, neutrophils but not peritoneal macrophages in vitro. Oxygen radical production by alveolar macrophages from SP-D +/+ and SP-D -/- mice was decreased following RSV infection and SP-D ameliorated the inhibitory effects of RSV on oxygen radical production by macrophages and neutrophils in vitro. Since the airway is the usual portal of entry for respiratory syncytial virus and other respiratory pathogens, the local production of SP-D is likely to play a role in innate defense responses to inhaled viruses.




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