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Suppression of cytokine expression by roflumilast and dexamethasone in a model of chronic asthma

机译：罗氟司特和地塞米松在慢性哮喘模型中抑制细胞因子表达

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摘要

Background: In a mouse model of mild chronic asthma, both inflammation and remodelling can be suppressed by dexamethasone (a glucocorticoid) and roflumilast (a selective phosphodiesterase-4 inhibitor). Objective: To better understand the underlying molecular mechanisms, we investigated the effects of treatment on airway expression of inflammation-related cytokines, as well as on epithelial expression of growth factors. Methods: BALB/c mice systemically sensitized to ovalbumin were challenged with aerosolized antigen for 6 weeks and treated with roflumilast or dexamethasone during the final 2 weeks. Expression of mRNA, for a variety of cytokines and growth factors, was assessed in selectively dissected proximal airways or in airway epithelium obtained by laser capture microdissection. Results: In the airway wall of vehicle-treated challenged animals, there was significantly elevated expression of mRNA for a variety of pro-inflammatory and T helper type 2 cytokines, as well as for IFN-?. All these cytokines were suppressed by dexamethasone. Treatment with roflumilast reduced expression of IL-17A, TNF-?, granulocyte- macrophage colony-stimulating factor and IL-6, but did not inhibit other cytokines. Both drugs suppressed the enhanced expression of mRNA for growth factors such as TGF-?and FGF-2 in airway epithelium. Conclusions: Whereas dexamethasone non-specifically inhibits numerous mediators involved in inflammation and the immune response, roflumilast selectively inhibits a subset of pro-inflammatory cytokines and growth factors. These mediators and/or the cells that produce them may have critical roles in the pathogenesis of the lesions of chronic asthma.
机译：背景：在轻度慢性哮喘的小鼠模型中，地塞米松（一种糖皮质激素）和罗氟司特（一种选择性磷酸二酯酶4抑制剂）可以抑制炎症和重塑。目的：为了更好地了解潜在的分子机制，我们研究了治疗对炎症相关细胞因子气道表达以及生长因子上皮表达的影响。方法：对全身对卵白蛋白致敏的BALB / c小鼠进行气雾化抗原攻击6周，并在最后2周内用罗氟司特或地塞米松治疗。在选择性解剖的近端气道或通过激光捕获显微切割术获得的气道上皮中，评估了多种细胞因子和生长因子的mRNA表达。结果：在接受媒介物处理的动物的气道壁中，各种促炎和2型T辅助细胞因子以及IFN-α的mRNA表达均明显升高。所有这些细胞因子均被地塞米松抑制。罗氟司特治疗可降低IL-17A，TNF-α，粒细胞巨噬细胞集落刺激因子和IL-6的表达，但不抑制其他细胞因子的表达。两种药物均抑制气道上皮中生长因子（如TGF-β和FGF-2）的mRNA表达增强。结论：地塞米松非特异性抑制多种炎症和免疫反应介质，而罗氟司特则选择性抑制部分促炎细胞因子和生长因子。这些介质和/或产生它们的细胞可能在慢性哮喘病变的发病机理中起关键作用。

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