Pulmonary surfactant proteins insert cation-permeable channels in planar bilayers.

Pulmonary surfactant, a mixture of lipids and proteins, promotes lung ventilation by reduction of surface tension at air-fluid interfaces. Exogenous surfactants containing hydrophobic proteins induce biological effects in lungs that are not fully explained by reduction of surface tension and are not induced by surfactants lacking proteins. We hypothesized that hydrophobic proteins from surfactant insert in membranes to induce channel activities that contribute to the observed biological effects of surfactant. To test for channel insertion by surfactant, planar lipid bilayers were monitored electrophysiologically in the presence of either intact pulmonary surfactant or extracted surfactant proteins reconstituted with phospholipids or directly added to bilayer lipids prior to membrane casting. In this in vitro model, both intact surfactant and extracted surfactant proteins initiated gated channel activities with slope conductances averaging 40 pS. Observed reversal potentials confirmed monovalent cation conductance, and conductance of smaller monovalent cations was selective. Voltage dependence of channel openings and rectification of channel current were not observed. These results confirm that hydrophobic surfactant proteins induce channel-mediated transport in artificial membranes. We speculate that pulmonary surfactants, in addition to reducing surface tension at air-fluid interfaces, initiate physiological and therapeutic effects in lung by cation channel insertion at exposed epithelial membranes.