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Am J Physiol Lung Cell Mol Physiol 287: L1199-L1206, 2004. First published July 30, 2004; doi:10.1152/ajplung.00457.2003
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Superoxide dismutase moderates basal and induced bacterial adherence and interleukin-8 expression in airway epithelial cells

Yuko Arita, Ansamma Joseph, Hshi-Chi Koo, Yuchi Li, Thomas A. Palaia, Jonathan M. Davis, and Jeffrey A. Kazzaz

CardioPulmonary Research Institute and the Departments of Medicine (Divisions of Pulmonary and Critical Care Medicine and Nephrology), Thoracic and Cardiovascular Surgery and Pediatrics (Neonatology), Winthrop-University Hospital, SUNY Stony Brook School of Medicine, Mineola, New York 11501

Submitted 31 December 2003 ; accepted in final form 21 July 2004

Bacterial infection of the tracheobronchial tree is a frequent, serious complication in patients receiving treatment with oxygen and mechanical ventilation, resulting in increased morbidity and mortality. Using human airway epithelial cell culture models, we examined the effect of hyperoxia on bacterial adherence and the expression of interleukin-8 (IL-8), an important mediator involved in the inflammatory process. A 24-h exposure to 95% O2 increased Pseudomonas aeruginosa (PA) adherence 57% in A549 cells (P < 0.01) and 115% in 16HBE cells (P < 0.01) but had little effect on Staphylococcus aureus (SA) adherence. Exposure to hyperoxia, followed by a 1-h incubation with SA, further enhanced PA adherence (P < 0.01), suggesting that hyperoxia and SA colonization may enhance the susceptibility of lung epithelial cells to gram-negative infections. IL-8 expression was also increased in cells exposed to both hyperoxia and PA. Stable or transient overexpression of manganese superoxide dismutase reduced both basal and stimulated levels of PA adherence and IL-8 levels in response to exposure to either hyperoxia or PA. These data indicate that hyperoxia increases susceptibility to infection and that the pathways are mediated by reactive oxygen species. Therapeutic intervention strategies designed to prevent accumulation of intracellular reactive oxygen species may reduce opportunistic pulmonary infections.

bacteria; inflammation; cytokines; antioxidants; adenovirus



Address for reprint requests and other correspondence: J. A. Kazzaz, CardioPulmonary Research Institute, 222 Station Plaza North, Suite 604, Mineola, NY 11501 (E-mail: jkazzaz{at}winthrop.org)







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