Distinct effects of surfactant protein A or D deficiency during bacterial infection on the lung

Mice lacking surfactant protein (SP)-A (SP-A(-/-)) or SP-D (SP-D-/-) and wi ld-type mice were infected with group B streptococcus or Haemophilus influe nzae by intratracheal instillation. Although decreased killing of group B s treptococcus and H. influenzae was observed in SP-A(-/-) mice but not in SP -D-/- mice, deficiency of either SP-A or SP-D was associated with increased inflammation and inflammatory cell recruitment in the lung after infection . Deficient uptake of bacteria by alveolar macrophages was observed in both SP-A- and SP-D-deficient mice. Isolated alveolar macrophages from SP-A(-/- ) mice generated significantly less, whereas those from SP-D-/- mice genera ted significantly greater superoxide and hydrogen peroxide compared with wi ld-type alveolar macrophages. In SP-D-/- mice, bacterial killing was associ ated with increased lung inflammation, increased oxidant production, and de creased macrophage phagocytosis. In contrast, in the absence of SP-A, bacte rial killing was decreased and associated with increased lung inflammation, decreased oxidant production, and decreased macrophage phagocytosis, Incre ased oxidant production likely contributes to effective bacterial killing i n the lungs of SP-D-/- mice, The collectins, SP-A and SP-D, play distinct r oles during bacterial infection of the lung.