Background: Pen ch 13 is an alkaline serine protease major allergen from Penicilliumchrysogenum. CD44 adhesion molecules play important roles in resolving lung inflammation and repairing epithelial damages during bronchial asthma. The purpose of this study was to investigate the effects of Pen ch 13 on CD44 of human bronchial epithelial cells.
Methods: Cells of the SV40-transformed immortalized bronchial epithelial cell line 16HBE14o- and primary cultures of human bronchial epithelial cells were exposed to purified Pen ch 13. CD44 expression on Pen ch 13-treated cells was analyzed by immunoblot analysis and flow cytometry. The release of soluble CD44 (sCD44) into culture supernatants was determined using human sCD44std ELISA kits.
Results: Pen ch 13 (0.01-1.0 μg/ml) dose-dependently down-regulates CD44 expression in 16HBE14o- cells. In addition, the decrease in CD44 expression can be abolished by pre-treating Pen ch 13 with a serine protease inhibitor, phenylmethyl-sulfonyl fluoride. Results from flow-cytometric analysis showed that the population mean fluorescence intensity for CD44 was significantly lower (p < 0.05) in Pen ch 13 (1.0 μg/ml)-treated 16HBE14o- cells (18 ± 4) than that of non-treated control cells (41 ± 7). Furthermore, Pen ch 13 induced increased shedding of sCD44 into the culture media compared with the shedding of non-treated 16HBE14o- and primary bronchial epithelial cells.
Conclusions: Pen ch 13 allergen down-regulated CD44 protein expression in airway epithelial cells. It may contribute to atopic asthma by influencing the resolution of lung inflammation and prolonging the repair response of damaged bronchial epithelial cells.
Copyright © 2010 S. Karger AG, Basel.