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Am. J. Respir. Crit. Care Med., Volume 163, Number 1, January 2001, 158-165

Surfactant Protein A Recruits Neutrophils into the Lungs of Ventilated Preterm Lambs

BORIS W. KRAMER, ALAN H. JOBE, CINDY J. BACHURSKI, and MACHIKO IKEGAMI

Department of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio

We tested the effects of surfactant protein A (SP-A) on inflammation and surfactant function in ventilated preterm lungs. Preterm lambs of 131 d gestation were ventilated for 15 min to initiate a mild inflammatory response, and were then treated with 100 mg/ kg recombinant human SP-C surfactant or with the same surfactant supplemented with 3 mg/kg ovine SP-A. Addition of SP-A to the SP-C surfactant did not change lung function. After 6 h of ventilation, cell numbers in the alveolar wash were 4.9 times higher in SP-A + SP-C-surfactant-treated animals. Cellular infiltrates consisted of neutrophils that produced less hydrogen peroxide than did cells from SP-C-surfactant-treated animals. Expression of adhesion molecules CD11b and CD44 was significantly greater after SP-A treatment, whereas the expression of CD14 was unchanged. Messenger RNAs (mRNAs) for the proinflammatory cytokines interleukin (IL)-1beta , IL-6, and IL-8, but not tumor necrosis factor-alpha , were increased in SP-A-treated lungs. Surfactant protein mRNAs and protein leakage into alveolar washes were not altered by SP-A, indicating that SP-A treatment produces no evidence of lung injury. The present study identifies an unanticipated role of SP-A in neutrophil recruitment in the lungs of preterm lambs.




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