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Korean J Asthma Allergy Clin Immunol. 2004 Dec;24(4):445-451. Korean. In Vitro.
Min TH , Lee BJ .
Department of Internal Medicine, School of Medicine, Sungkyunkwan University and Samsung Medical Center, Seoul, Korea. dcchoi@smc.samsung.co.kr
Abstract

BACKGROUND: Eotaxin has been identified as a key mediator of tissue eosinophil inflammation in asthma or allergic rhinitis. However, the concentration of tissue eotaxin is not elevated in asthmatic patients. Therefore, we hypothesized that some other materials such as proinflammatory cytokines are essential in allergic inflammation affected by eotaxin. OBJECTIVE: The aim of this study was to establish the influence of eotaxin in vitro on the nitric oxide, which is a marker of pulmonary inflammation in asthma. METHOD: A549 cells were cultured and stimulated with tumor necrosis factor-alpha (TNF-alpha ), interleukin-1beta (IL-1beta), interferon-gamma (IFN-gamma), and eotaxin in various combined concentration. The concentration of supernatant nitrite was analyzed with Griess reaction method and the expression of inducible nitric oxide synthase (iNOS) was evaluated using a reverse transcriptase polymerase chain reaction (RT-PCR) assay. RESULT: Only the groups stimulated with both eotaxin and the mixture of TNF-alpha, IL-1beta, and IFN-gamma showed the increase of the concentration of supernatant nitrite (P <0.05) and iNOS expression. In addition, with the mixture of TNF-alpha, IL-1beta, and IFN-gamma, the concentration of supernatant nitric oxide was correlated to the concentration of the stimulated eotaxin (correlation coeffient=0.592, P <0.05). CONCLUSION: Eotaxin, together with TNF-alpha, IL-1beta, and IFN-gamma, could make bronchial epithelial cells (A549) produce nitric oxide and augment the production of nitric oxide.

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