Oxidant-injured airway epithelial cells upregulate thioredoxin but do not produce interleukin-8

Karen L. Oslund, Lisa Miller, Jodie L. Usachenko, Nancy K. Tyler, Reen Wu, Dallas M. Hyde

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

We tested the hypothesis that oxidant-injured cells upregulate thioredoxin, whereas oxidant-stressed, but not injured, cells upregulate interleukin (IL)-8 after injury. We exposed primary human tracheobronchial epithelial cells and transformed human bronchial epithelial cells (BEAS-2B S.6) to 0, 200, 400, or 600 μM H2O2 for 1 h followed by an additional 7 h of incubation. Subsequently, the cells were double-labeled with markers of injury (either Ethidium Homodimer-1 for cellular injury or MitoTracker dye for functional mitochondria) or oxidant stress (5-[and 6]-chloromethyl-2′, 7′-dicholorodihydrofluorescein diacetate) and antibodies specific for the chemoattractants IL-8 or thioredoxin. We found significant inverse relationships between numbers and stained chemoattractant volumes of IL-8 and thioredoxin-positive cells with increasing H2O2 dose. Cells with mitochondrial injury produced thioredoxin but not IL-8, and oxidant-stressed cells were more likely to produce thioredoxin than IL-8. isolated human neutrophils were more likely to colocalize with thioredoxin-positive BEAS-2B S.6 cells than thioredoxin-negative cells. The H2O2 injury did not induce significant apoptosis in the BEAS-2B S.6 cells as measured by caspase 3 activation. We conclude that oxidant-injured and stressed airway epithelial cells upregulate thioredoxin, but produce little IL-8, which may be important in airway epithelial cell-mediated multistep navigation of neutrophils to sites of oxidant injury.

Original languageEnglish (US)
Pages (from-to)597-604
Number of pages8
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume30
Issue number5
DOIs
StatePublished - May 2004

ASJC Scopus subject areas

  • Cell Biology
  • Pulmonary and Respiratory Medicine
  • Molecular Biology

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