Surfactant protein-A binds group B Streptococcus enhancing phagocytosis and clearance from lungs of surfactant protein-A-deficient mice

Surfactant protein-A (SP-A) gene-targeted mice clear group B streptococcus (GBS) from the lungs at a slower rate than wild-type mice. To determine mec hanisms by which SP-A enhances pulmonary clearance of GBS, the role of SP-A in binding and phagocytosis of GES was assessed in SP-A (-/-) mice infecte d with GBS in the presence and absence of exogenous SP-A. Coadministration of GBS with exogenous SP-A decreased GBS colony counts in lung homogenates of SP-A (-/-) mice. SP-A bound to GBS in a calcium-dependent manner. Althou gh pulmonary infiltration with macrophages was not altered in SP-A (-/-) ve rsus wild-type mice after GBS infection, the number of alveolar macrophages with phagocytosed bacteria was lower in the SP-A (-/-) mice than in the wi ld-type mice. When SP-A was coadministered with GBS, phagocytosis was signi ficantly increased. Oxygen radical production by alveolar macrophages from SP-A (-/-) mice infected with GBS was decreased compared with wild-type con trols and was in creased when SP-A (-/-) mice were infected in the presence of exogenous SP-A. Superoxide (SO) radical generation was deficient in mac rophages from SP-A (-/-) mice. SP-A plays an important role in GBS clearanc e in vivo, mediated in part by binding to and enhancing GBS phagocytosis an d by increasing SO production by alveolar macrophages.