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The role of oxidative stress in rhinovirus induced elaboration of IL-8 by respiratory epithelial cells
Institution:1. Department of Pediatrics, Medical University of South Carolina, Charleston, SC, USA;1. Department of Experimental Medicine University of Perugia, 06129 Perugia, Italy;2. Department of Medicine, School of Medicine, University of Perugia, 06129 Perugia, Italy;1. Bawaskar Hospital and Clinical Research Center, Mahad 402301, India;1. Department of Analytical Chemistry, China Pharmaceutical University, 24 Tongjia Lane, Gulou District, Nanjing, 210009, China;2. Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of Education, 24 Tongjia Lane, Gulou District, Nanjing, 210009, China;1. National Institute for Occupational Safety and Health (NIOSH), Nanotechnology Research Center (NTRC), Cincinnati, OH 45226, USA;2. West Virginia University, Department of Industrial and Management System Engineering, Morgantown, WV 26506, USA
Abstract:A direct correlation has been reported between the severity of symptoms associated with rhinovirus infection and the concentration of interleukin-8 in nasal secretions. The purpose of these studies was to examine the mechanism of rhinovirus-induced IL-8 elaboration. Rhinovirus infection induced oxidative stress in Beas-2b cells and the concentration of H2O2 in supernatant media from rhinovirus challenged cells was 12.5 ± 6.1 μM 1 h after challenge compared to 0.7 ± 0.3 μM in supernatant from control cells. N-acetyl cysteine inhibited RV-induced NF-κB activation and IL-8 elaboration. IL-8 concentrations were 36 ± 2 pg/ml and 10 ± 1 pg/ml 6 h after virus challenge in untreated and NAC-treated (30 mM NAC) cells, respectively. Despite the effects of NAC on IL-8 elaboration and NF-κB activation, RV stimulated increases in supernatant H2O2 were not altered by NAC. These data suggest that RV stimulation of IL-8 in respiratory epithelium is mediated through production of oxidative species and the subsequent activation of NF-κB.
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