Surfactant Protein-A-Deficient Mice Are Susceptible toPseudomonas aeruginosaInfection

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Abstract
To determine the role of surfactant protein-A (SP-A) in host defense, the murine SP-A locus was targeted by homologous recombination to produce mice lacking SP-A. SP-A−/− and wild-type mice were infected with mucoid Pseudomonas aeruginosa by intratracheal instillation. Pulmonary bacterial loads were greater in SP-A−/− than in wild-type mice, with increased numbers of mucoid P. aeruginosa in lung homogenates at 6 and 24 h after infection. Pulmonary infiltration with polymorphonuclear leukocytes (PMN) was similar in both groups; however, an earlier influx of PMN into the lung occurred in the SP-A−/− mice. The number of bacteria phagocytosed by alveolar macrophages was decreased in the SP-A−/− mice at 1 h after infection. Superoxide-radical generation by PMN was similar for the SP-A−/− and wild-type mice, but nitrite levels were increased in SP-A−/− mice. Concentrations of tumor necrosis factor-α, interleukin-6, and macrophage inflammatory protein-2 (proinflammatory cytokines) were greater in bronchoalveolar...