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Children's Hospital Medical Center, Division of Neonatology and Pulmonary Biology, Cincinnati, Ohio 45229
Surfactant protein A (SP-A) is a member of the
collectin family of host defense molecules expressed primarily in the
epithelial cells of the lung. To determine the role of SP-A in
pulmonary adenoviral infection, SP-A-deficient (SP-A 
/)
mice were intratracheally infected with a replication-deficient
recombinant adenovirus, Av1Luc1. Lung inflammation was markedly
increased in SP-A / compared with SP-A +/+ mice and was
associated with increased hemorrhage and epithelial cell injury.
Polymorphonuclear cells in bronchoalveolar lavage fluid (BALF) were
increased in SP-A / mice after administration of
adenovirus. Coadministration of adenovirus and purified human SP-A
ameliorated adenoviral-induced lung inflammation in SP-A
/ mice. Concentrations of tumor necrosis factor-
(TNF-), interleukin (IL)-6, and IL-1
were increased in BALF of
SP-A / mice. Likewise, TNF-, IL-6, macrophage
inflammatory protein (MIP)-1, monocyte chemotactic protein-1, and
MIP-2 mRNAs were increased in lung homogenates from SP-A
/ mice 6 and 24 h after viral administration. Clearance
of adenoviral DNA from the lung and uptake of fluorescent-labeled
adenovirus by alveolar macrophages were decreased in SP-A
/ mice. SP-A enhances viral clearance and inhibits lung
inflammation during pulmonary adenoviral infection, providing support
for the importance of SP-A in antiviral host defense.
surfactant protein A; lung epithelium; collectins; alveolar macrophages
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