Abstract
Exposure of 2-chloroethyl ethyl sulfide (CEES) to guinea pigs causes lung injury by infiltration of neutrophils in interstitial lung spaces. A unique MAPK-regulated transcription factor, C/EBP (CCAAT-enhancer-binding protein), regulates the expression of intracellular adhesion molecule-1 (ICAM-1), involved in recruiting neutrophils in lung. The present study was to determine if CEES exposure causes activation of C/EBP, in particular the predominant β-isoform and if so whether it can be prevented by intratracheal delivery of an antioxidant liposome containing N-acetyl cysteine and tocopherols. Lung injury was developed in guinea pigs by intratracheal exposure of CEES (0.5 mg/kg). The antioxidant liposome was given intratracheally 5 min after CEES exposure, and the animals were sacrificed after 30 days. CEES exposure caused a 2.3-fold increase in the activation of C/EBP accompanied with a 45% and 121% increase in the protein level of C/EBP β and ICAM-1, respectively, and this effect was counteracted by the antioxidant liposome.