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首页> 外文期刊>Pulmonary pharmacology & therapeutics >Kinetics of airway hyperresponsiveness and airway eosinophilia in BALB/c mice and their modulation by different dexamethasone treatment regimens.
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Kinetics of airway hyperresponsiveness and airway eosinophilia in BALB/c mice and their modulation by different dexamethasone treatment regimens.

机译：BALB / c小鼠气道高反应性和气道嗜酸性粒细胞的动力学及其通过不同地塞米松治疗方案的调节。

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摘要

The mechanisms of airway hyperresponsiveness (AHR) are still poorly understood. In this study we have established a model of persistent AHR and eosinophilia and evaluated the prophylactic vs. therapeutic effects of dexamethasone on these parameters. Mice were immunised with ovalbumin (OVA) on day 0 and challenged intranasally on days 10, 11, 12 and 13 with OVA or phosphate buffer saline (PBS). Airway responsiveness to methacholine, measured 24-h post multiple intranasal OVA challenges, was significantly increased compared to time matched PBS-controls (P<0.05). AHR could be detected for up to 14 days after the last OVA challenge although the magnitude of the AHR had diminished by day 14 compared to day 1. OVA challenge of mice induced a significant airway eosinophilia at 24h (P<0.05); this persisted for 2 weeks after the challenge. Prophylactic treatment with dexamethasone (1mg x kg (-1)) reduced the OVA induced AHR, eosinophilia and mucus cell hyperplasia/metaplasia measured 24h post challenge. Therapeutic treatment, with dexamethasone (2 mg x kg(-1)), significantly inhibited established airway eosinophilia, measured at 72 h post OVA challenge, only when treatment was initiated at 24h but not 48 h after challenge. In contrast, AHR measured at 72 h post OVA challenge was significantly reduced when treatment was started at either 24 or 48 h post challenge. Our data shows that the immunization and challenge procedures employed resulted in a persistent type of AHR. Prophylactic intervention with steroids almost completely inhibited its development; however therapeutic intervention only partially resolved AHR.
机译：气道高反应性（AHR）的机制仍知之甚少。在这项研究中，我们建立了持续性AHR和嗜酸性粒细胞增多的模型，并评估了地塞米松对这些参数的预防作用与治疗作用。在第0天用卵清蛋白（OVA）免疫小鼠，并在第10、11、12和13天鼻内用OVA或磷酸盐缓冲盐水（PBS）攻击。与时间匹配的PBS对照相比，多次鼻内OVA刺激后24小时测得的气道对乙酰甲胆碱的反应性显着提高（P <0.05）。尽管与第1天相比，到第14天AHR的强度已降低，但最后一次OVA攻击后长达14天仍可检测到AHR。24小时后，小鼠的OVA攻击诱导了明显的气道嗜酸性粒细胞增多（P <0.05）;挑战后持续2周。地塞米松（1mg x kg（-1））的预防性治疗可降低激发后24小时测得的OVA诱导的AHR，嗜酸性粒细胞增多和粘液细胞增生/间质转移。仅在攻击后24小时开始治疗，而在攻击后48小时才开始使用地塞米松（2 mg x kg（-1））的治疗性治疗可显着抑制既定的气道嗜酸性粒细胞增多（在OVA攻击后72小时测得）。相反，在激发后24或48小时开始治疗时，OVA激发后72小时测得的AHR显着降低。我们的数据表明，所采用的免疫和激发程序导致了AHR的持续存在。类固醇的预防性干预几乎完全抑制了其发展。然而，治疗性干预只能部分解决AHR。

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