We tested the hypothesis that oxidant-injured cells upregulate thioredoxin, while oxidant-stressed, but not injured, cells upregulate 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 600µM H₂0₂ for 1 hour followed by an additional 7 hours 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 H₂0₂ 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 co-localize with thioredoxin positive BEAS-2B S.6 cells than thioredoxin negative cells. The H₂0₂ 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.