Mice lacking surfactant protein surfactant protein. D (SP-D-/-) and wild-ty
pe mice (SR-D+/+) were infected with influenza A virus (IAV) by intranasal
instillation.. IAV infection increased the endogenous SP-D concentration in
wild-type mice. SP-D-deficient mice showed decreased viral clearance of th
e Phil/82 strain of IAV and increased production of inflammatory cytokines
in response to viral challenge. However, the less glycosylated strain of UV
, Mem/71, which is relatively resistant to SP-D in vitro, was cleared effic
iently from the lungs of SP-D-/- mice. Viral clearance of the Phil/82 strai
n of IAV and the cytokine response were both normalized by the coadministra
tion of recombinant SP-D. Since the airway is the usual portal of entry for
influenza A virus and other respiratory pathogens, SP-D is likely to play
an important role in innate defense responses to IAV.