Abstract
BACKGROUND: Liquid ventilation is associated with decreased inflammatory response in an injured
lung. This study was performed to investigate if whether perfluorocarbon (PFC) can decrease
chemokine expression in airway epithelial cells. METHODS : A549 cells were used for airway
epithelial cells and perfluorodecalin for PFC. To expose cells to PFC, lower chamber of
Transwell a plate was used. This study was performed in two parts. In the first part, we
examined whether PFC could decrease chemokine expression in airway epithelial cells through
inhibition of other inflammatory cells. Peripheral blood mononuclear cells (PBMC's) were
isolated and stimulated with lipopolysaccharide (LPS, 10 mg/mL) for 24 hours with or without
exposure to PFC. Then A549 cells were stimulated with conditioned media (CM) containing the
culture supernatants of PBMC . After 24 hours, the expressions of interleukin-8 (IL-8) and
RANTES were measured. In the second part of the study, we studied whether PFC could directly
suppress chemokine expression in airway epithelial cells. A549 cells were stimulated for 24
hours with interleukin-1b and/or tumor necrosis factor-a with or without exposure to
PFC (,)and then the chemokine expression was measured. Northern analysis was used to
measure the mRNA expression (,) and ELISA was used for immunoreactive protein measurements
in culture supernatant. RESULTS: 1. IL-8 and RANTES mRNA expression and immunoreactive
protein production were increased significantly by CM from LPS-stimulated PBMC in A459
cells compared with CM from unstimulated PBCM(p<0.05) (,)but exposure of PFC had no
significant effect on either mRNA expression immunoreactive protein expression. 2. IL-8 and
RANTES mRNA expression and immunoreactive protein production were increased significantly by
IL-1b and TNF-a in A549 cells(p<0.05)(,)but exposure of PFC had no significant effect on
either mRNA expression or immunoreactive protein production.
CONCLUSION: Decreased chemokine expression of airway epithelial cells may not be involved in
decreased inflammatory response observed in liquid ventilation. Further studies on possible
mechanisms of decreased inflammatory response are warranted.