Tuberc Respir Dis > Volume 54(1); 2003 > Article
Tuberculosis and Respiratory Diseases 2003;54(1):104-113.
DOI: https://doi.org/10.4046/trd.2003.54.1.104    Published online January 1, 2003.
The Role of Interleukin 8 and NF(nuclear factor)-kappaB in Rhinovirus-Induced Airway Inflammation.
Ho Joo Yoon, Mi Ok Kim, Jang Won Sohn, Jung Mogg Kim, Dong Ho Shin, Sung Soo Park
1Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea. hjyoon@hanyang.ac.kr
2Department of Microbiology, Hanyang University College of Medicine, Seoul, Korea.
Abstract
BACKGROUND
Rhinovirus(RV) infections frequently trigger dyspnea and paroxysmal cough in adult patients with asthma and are the most prevalent cause of the common cold. However, the mechanisms of a RV-induced airway inflammation is unclear. Since the RV does not directly destroy the airway epithelium, it is presumed that the immune response to the RV contributes to the pathogenesis of the respiratory symptoms. In order to test this hypothesis, this study characterized the time-sequenced alterations in interleukin(IL)-8 elaboration from the human bronchial epithelial cells and evaluated the role of NF(nuclear factor)-kappaB in the RV-induced IL-8 production by pretreating the inhibitors of NF-kappaB activation. METHODS: The ability of RV-infected human bronchial epithelial cells and BEAS-2B cells to produce the IL-8 was compared with the controls. This study infected BEAS-2B cells with the RV14 obtained from the American Type Culture Collection. The supernatants were harvested from the RV infected BEAS-2B cells and the controls at 2hr, 4hr, 6hr, 12hr, 24hr, 48hr from the inoculation time. This study measured the IL-8 concentration using the ELISA kits. In order to elucidate the role of NF-kappaB in the RV-induced IL-8 production, the effect of the NF-kappaB inhibitors was evaluated on RV-induced IL-8 production. RESULTS: The BEAS-2B cells produced small amounts of IL-8 that accumulated slowly with time in the culture. The RV was a potent stimulator of the IL-8 proteins production by BEAS-2B human bronchial epithelial cells. Antioxidants, N-acetyl-L-cysteine(NAC),\ and pyrrolidine dithiocarbamate(PDTC), blocked the IL-8 elaboration by the RV-infected BEAS-2B cells, which was dose-dependent, but N-Tosyl-L-phenylalanine chloromethyl ketone(TPCK) did not. CONCLUSION: Some antioxidants inhibited the RV-induced IL-8 production by blocking the NF-kappaB, which may have a therapeutic potential in asthma.
Key Words: IL-8, Rhinovirus, Antioxidants, NF-kappaB
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