Introduction: The potential role of polymorphonuclear neutrophils(PMN) and macrophages in the pathogenesis of acute respiratory distress syndrome (ARDS) develops as a result of CD 62 L (L-selectin) mediated inflammatory-cell endothelial injury. Surfactant (SF) replacement therapy is gaining increased use in term infants and adults with ARDS. We therefore wanted to determine the effect of SF on CD 62-L expression of PMN and monocytes. Material and methods: Heparinized whole blood (5 ml) from healthy adult volunteers was incubated for 1 hour with 10-6 mol/ml N-formylmethionyl-leucylphenylalanin (fMLP) together with bovine SF(Alveofact®; Fa. Thomae, F.R.G.) and synthetic SF (Exosurf®, Wellcome, USA) (1,2 mg/ml). Elastase-α1 - proteinase inhibitor complex(E-PI) as a result of PMN-activation was determined by chemoluminescence immunoassay. Analyses of PMN and monocytes population as well as CD 62 L expression were performed on a FACScan flow cytometer (Becton Dickinson, F.R.G.). CD 62 L were expressed as percentage of positive stained cells.Results: After incubation with natural SF and fMLP decreased E-PI levels from 30% compared with E-PI levels after incubation with fMLP alone. Increased levels of E-PI of 90% after incubation with synthetic surfactant were found: Table Conclusion: In contrast to synthetic SF natural SF is able to inhibit PMN activation in vitro. After incubation with SF CD 62 L-expression is decreased, depending on the preparation used. From our data we conclude that SF treatment can influence inflammatory cell-mediated endothelial cell injury in the early stage of acute lung injury.

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