Pollutant particles induce arginase II in human bronchial epithelial cells.

Journal Article (Journal Article)

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 μM), 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.

Full Text

Duke Authors

Cited Authors

  • Hyseni, X; Soukup, JM; Huang, Y-CT

Published Date

  • 2012

Published In

Volume / Issue

  • 75 / 11

Start / End Page

  • 624 - 636

PubMed ID

  • 22712848

International Standard Serial Number (ISSN)

  • 1528-7394

Digital Object Identifier (DOI)

  • 10.1080/15287394.2012.688479


  • eng

Conference Location

  • England