We tested the effects of surfactant protein A (SP-A) on inflammation and su
rfactant function in ventilated preterm lungs, Preterm lambs of 131 d gesta
tion were ventilated for 15 min to initiate a mild inflammatory response, a
nd were then treated with 100 mg/ kg recombinant human SP-C surfactant or w
ith the same surfactant supplemented with 3 mg/kg ovine SP-A. Addition of S
P-A to the SP-C surfactant did not change lung function. After 6 h of venti
lation, cell numbers in the alveolar wash were 4.9 times higher in SP-A + S
P-C-surfactant-treated animals. Cellular infiltrates consisted of neutrophi
ls that produced less hydrogen peroxide than did cells from SP-C-surfactant
-treated animals. Expression of adhesion molecules CD11b and CD44 was signi
ficantly greater after SP-A treatment, whereas the expression of CD14 was u
nchanged. Messenger RNAs (mRNAs) for the proinflammatory cytokines interleu
kin (IL)-1 beta, IL-6, and IL-8, but not tumor necrosis factor-alpha, were
increased in SP-A-treated lungs. Surfactant protein mRNAs and protein leaka
ge into alveolar washes were not altered by SP-A, indicating that SP-A trea
tment produces no evidence of lung injury. The present study identifies an
unanticipated role of SP-A in neutrophil recruitment in the lungs of preter
m lambs.