You are here:
Pollutant particles induce arginase II in human bronchial epithelial cells
Citation:
Hyseni, X., J. Soukup, AND Y. Huang. Pollutant particles induce arginase II in human bronchial epithelial cells. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES 75(11):624-636, (2012).
Impact/Purpose:
Arginase has been shown to play an important role in the pathogenesis of asthma. In this study, we hypothesized that particulate matter exposure would induce arginase.
Description:
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, we hypothesized that PM exposure would induce arginase. Human bronchial epithelial cells (HBEC) obtained from normal individuals by endobronchial brushings cultured on air-liquid interface were incubated with fine Chapel Hill particles (PM2.5, 100 ug/ml) for up to 72 hours. Arginase activity, protein expression and mRNA of arginase I and II were measured. PM2.5 increased arginase activity in a time-dependent manner. The increase was primarily due to upregulation of arginase II. PD153035 (10 uM), an epidermal grow factor (EGF) receptor antagonist, attenuated the PM2.5-induced increase 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 ug/ml), an NAD(P)H oxidase inhibitor, did not 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 in human bronchial epithelial cells, in part via EGF-dependent mechanisms independent of oxidative stress. The increased arginase II may be a mechanism for adverse effects induced by PM exposure in asthma patients.