Inhibition of airways inflammation by dexamethasone is followed by reduced bronchial hyperreactivity in BP2 mice
Inhibition of airways inflammation by dexamethasone is followed by reduced bronchial hyperreactivity in BP2 mice
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DOI：
10.1046/j.1365-2222.1996.d01-398.x
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发表时间：
1996-08-01
影响因子：
6.1
通讯作者：
Vargaftig, BB
中科院分区：
文献类型：
--
作者：
Eum, SY;Creminon, C;Vargaftig, BB
背景气道炎症细胞浸润是哮喘的一个恒定特征，被认为是导致支气管高反应性的原因。（BHR）。我们最近开发了一种BHR模型，使用选择的小鼠，命名为BP 2，其显示嗜酸性粒细胞依赖性BHR抗原攻击后。抗IL-5抗体可抑制抗原诱导的嗜酸性粒细胞（EOS）向BP 2小鼠气道的聚集及BHR。目的探讨炎症细胞浸润在BHR诱导中的作用。方法观察糖皮质激素地塞米松对气道EOS及BHR的影响。结果地塞米松1.25 mg/kg（10 mg/kg）可明显抑制BHR诱导的EOS向气道的聚集及BHR的升高。结论IL-5抗体可抑制BP 2小鼠气道EOS的聚集及BHR的升高。在四种抗原激发前1小时，腹腔注射1 kg，抑制气道嗜酸性粒细胞增多和BHR对静脉内5-HT和雾化乙酰甲胆碱的反应，以及BALF和血清中IL-5的产生。相比之下，地塞米松未能减少过敏性bronchoconstrictions.Conclusions这些结果表明，地塞米松发挥其抑制抗原诱导的小鼠气道嗜酸性粒细胞增多症的影响，通过抑制IL-5的产生，但它不阻止过敏性介质在小鼠中的释放。
Background Infiltration of inflammatory cells in the airways is a constant characteristic of asthma and is considered to result in bronchial hyperreactivity.(BHR). We have recently developed a model of BHR using a selection of mice, named BP2, which display eosinophil-dependent BHR following antigen challenges. An anti-IL-5 antibody suppressed antigen-induced eosinophil recruitment to the airways and BHR in BP2 mice.Objective To investigate the implication of infiltrated inflammatory cells in the induction of BHR in mice.Methods The effects of glucocorticosteroid dexamethasone on airways eosinophilia and BHR were observed.Results Administration of dexamethasone at the dose of 1.25 mg/kg i.p. 1 h before each of four antigen provocations suppressed the airways eosinophilia and BHR in response to intravenous 5-HT and to aerosolized methacholine, as well as IL-5 production in the BALF and in the serum. By contrast, dexamethasone failed to reduce anaphylactic bronchoconstriction.Conclusions These results suggest that dexamethasone exerts its inhibitory effects on antigen-induced airways eosinophilia in mice by inhibiting IL-5 production, but that it does not block the liberation of anaphylactic mediators in mice.