|Title:||Interleukin-12 Inhibits Eotaxin Secretion of Cultured Primary Lung Cells and Alleviates Airway Inflammation in Vivo||Authors:||CHIANG, BOR-LUEN||Keywords:||eotaxin;interferon-gamma;interleukin-12;lung cell culture||Issue Date:||2002||Journal Volume:||v.19||Journal Issue:||n.2||Start page/Pages:||76-84||Source:||CYTOKINE||Abstract:||
The mechanisms that cause the inflammation of airway and lung tissue in asthma have been studied extensively. It is noted that type 1 T helper cell (Th1)-related cytokines could decrease the accumulation of eosinophils in lung tissue and relieve airway constriction. But the therapeutic mechanisms of Th1 cytokines remain unclear. In this study, interleukin-12 (IL-12) DNA plasmid as a therapeutic reagent was delivered intravenously. Bronchoalveolar lavage (BAL) fluids were collected from IL- 12 treated and control mice, and analyzed for cell composition and eotaxin level. The results showed that IL-12 DNA plasmid could effectively inhibit eosinophilia and airway inflammation in vivo. The level of eotaxin in BAL fluid also decreased. To further investigate the effect of Th1- related cytokines, such as IL- 12 or interferon-gamma (IFN-gamma) on the eotaxin level produced by lung cells, primary lung cell culture was established. The results demonstrated that both IL-12 and IFN-gamma could suppress eotaxin secretion from IL-13 or IL- 4 stimulated primary lung cell culture. Moreover, the inhibitory effect of IL-12 could not be reversed by the administration of anti-IFN-gamma antibody. All the evidences suggested that IL-12 could regulate airway inflammation by suppressing the eotaxin secretion of lung tissue through an IFN-gamma independent mechanism. (C) 2002 Elsevier Science Ltd. All rights reserved.
|Appears in Collections:||醫學系|
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