Hypochlorous acid alters bronchial epithelial cell membrane properties and prevention by extracellular glutathione

Charles J. Venglarik, Julio Girón-Calle, Amanda F. Wigley, Ernst Malle, Nobuo Watanabe, Henry Jay Forman

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)


In chronic inflammatory diseases of the airways, such as cystic fibrosis, hypochlorous acid (HOCl) generated by neutrophils is involved in airway injury. We examined the effects of HOC1 on 16HBE14o- bronchial epithelial cells by bolus addition or by generation with glucose oxidase plus myeloperoxidase. HOC1 produced both carbonyl formation of a discreet number of proteins and modification of surface targets that were recognized by an antibody raised against HOCl-modified protein. Bolus or enzymatically generated HOCl decreased transepithelial resistance, but surprisingly bolus HOCl also increased short-circuit current. Glutathione in lung epithelial lining fluid is an excellent scavenger of HOCl; however, glutathione content is lower in cystic fibrosis epithelial lining fluid due to deficient glutathione transport to the apical side of bronchial-tracheal epithelial cells (Gao L, Kim KJ, Yankaskas JR, and Forman HJ. Am J Physiol Lung Cell Mol Physiol 277: L113-L118, 1999). We found that alteration of the GSH content of apical fluid above 16HBE14o- cells was protective because all HOCl-induced changes were delayed or eliminated by exogenous glutathione within the physiological range. Extrapolating this to cystic fibrosis suggests that HOC1 can alter cell function without destruction but that elevating glutathione could be protective.

Original languageEnglish
Pages (from-to)2444-2452
Number of pages9
JournalJournal of Applied Physiology
Issue number6
Publication statusPublished - 2003 Dec


  • 16HB14o- cells
  • Epithelial lining fluid

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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