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Surfactant Proteins A and D Enhance Pulmonary Clearance of Pseudomonas aeruginosa

Department of Pediatrics, Cardiovascular Research Institute, and Department of Anesthesia, University of California San Francisco, San Francisco, California

Correspondence and requests for reprints should be addressed to Sam Hawgood, Room M-696, 505 Parnassus Avenue, University of California San Francisco, San Francisco, CA 94143-0110. E-mail: hawgoods{at}peds.ucsf.edu

Surfactant protein (SP)-A and SP-D, members of the collectin family, are involved in innate host defenses against various bacterial and viral pathogens. In this study, we asked whether SP-A and SP-D enhance clearance of a nonmucoid strain of Pseudomonas aeruginosa from the lungs. We infected mice deficient in SP-A (SP-A–/–), SP-D (SP-D–/–) and both pulmonary collectins (SP-AD–/–) by intratracheal administration of P. aeruginosa. Six hours after infection, bacterial counts were significantly higher in SP-A–/–, SP-D–/–, and SP-AD–/– compared with wild-type (WT) mice. Forty-eight hours after infection, bacterial counts were significantly higher in SP-A–/– mice compared with WT mice and in SP-AD–/– mice compared with WT, SP-A–/–, and SP-D–/– mice. Phagocytosis of the bacteria by alveolar macrophages was decreased in SP-A–/– and SP-D–/– mice. Levels of macrophage inflammatory peptide–2 and IL-6 were more elevated in the lungs of SP-D and SP-AD–/– mice compared with WT mice. There was more infiltration by neutrophils in the lungs of SP-D–/– compared with WT and SP-A–/– mice 48 h after infection. This study shows that SP-A and SP-D enhance pulmonary clearance of P. aeruginosa by stimulating phagocytosis by alveolar macrophages and by modulating the inflammatory response in the lungs. These findings also show that the functions of SP-A and SP-D are not completely redundant in vivo.

Key Words: pneumonia • Pseudomonas aeruginosa • surfactant proteins

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