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Abstract
Exposure to particulate matter (PM) is associated with adverse pulmonary effects, including induction and exacerbation of asthma. Recently arginase was shown to play an important role in the pathogenesis of asthma. In this study, it was postulated that PM exposure might induce arginase. Human bronchial epithelial cells (HBEC) obtained from normal individuals by endobronchial brushings cultured on an air–liquid interface were incubated with fine Chapel Hill particles (PM2.5, 100 μg/ml) for up to 72 h. Arginase activity, protein expression, and mRNA of arginase I and arginase II were measured. PM2.5 increased arginase activity in a time-dependent manner. The rise was primarily due to upregulation of arginase II. PD153035 (10 μ M), an epidermal growth factor (EGF) receptor antagonist, attenuated the PM2.5-induced elevation in arginase activity and arginase II expression. Treatment of HBEC with human EGF increased arginase activity and arginase II expression. Pretreatment with catalase (200 U/ml), superoxide dismutase (100 U/ml), or apocynin (5 μg/ml), an NAD(P)H oxidase inhibitor, did not markedly affect arginase II expression. Treatment of HBEC with arginase II siRNA inhibited the expression of arginase II by 60% and increased IL-8 release induced by PM2.5. These results indicate that PM exposure upregulates arginase II activity and expression in human bronchial epithelial cells, in part via EGF-dependent mechanisms independent of oxidative stress. The elevated arginase II activity and expression may be a mechanism underlying adverse effects induced by PM exposure in asthma patients.
Acknowledgments
The research described in this article was funded by the intramural grant of the U.S. Environmental Protection Agency (EPA). It has been reviewed by the U.S. EPA and the contents do not necessarily reflect the views and policies of the U.S. EPA, nor does mention of the trade names or commercial products constitute endorsement or recommendation for use.