Published ahead of print on April 28, 2005, doi:10.1165/rcmb.2004-0365OC Am. J. Respir. Cell Mol. Biol., Volume 33, Number 2, August 2005, 161-168 A more recent version of this article appeared on August 1, 2005
Submitted on November 22, 2004 Lung Surfactant Gelation Induced by Epithelial Cells Exposed to Air Pollution or Oxidative StressJay W Anseth1,1 Department of Chemical Engineering, Stanford University Medical Center, Stanford, CA, USA, 2 Pulmonary and Critical Care Medicine, NHEERL, EPA, Research Triangle Park, NC, USA, 3 Department of Pulmonary and Critical Care Medicine, Stanford University Medical Center, Stanford, CA, USA * To whom correspondence should be addressed. E-mail: peterkao{at}stanford.edu.
Lung surfactant lowers surface tension and adjusts interfacial rheology to facilitate breathing. A novel instrument, the interfacial stress rheometer (ISR), utilizes an oscillating magnetic needle to measure the shear viscosity and elasticity of a surfactant monolayer at the air-water interface. The ISR reveals that calf lung surfactant, Infasurf, exhibits remarkable fluidity, even when exposed to air pollution residual oil fly ash (ROFA), hydrogen peroxide (H2O2), or conditioned media from resting A549 alveolar epithelial cells (AEC). However, when Infasurf is exposed to a subphase of the soluble fraction of ROFA- or H2O2-treated AEC conditioned media, there is a prominent increase in surfactant elasticity and viscosity, representing two-dimensional gelation. Surfactant gelation is decreased when ROFA-AEC are pretreated with inhibitors of cellular reactive oxygen species (ROS), or with a mitochondrial anion channel inhibitor, as well as when A549-
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0 cells that lack mitochondrial DNA and functional electron transport are investigated. These results implicate both mitochondrial and non-mitochondrial ROS generation in ROFA-AEC-induced surfactant gelation. A549 cells treated with H2O2 demonstrate a dose-dependent increase in lung surfactant gelation. The ISR is a unique and sensitive instrument to characterize surfactant gelation induced by oxidatively-stressed AEC.
