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首页> 外文期刊>International medical journal: IMJ >Monoclonal Antibody against IL-5 Receptor Alpha, but Not IL-5, Inhibits Airway Hyperresponsiveness Associated with Airway Remodeling
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Monoclonal Antibody against IL-5 Receptor Alpha, but Not IL-5, Inhibits Airway Hyperresponsiveness Associated with Airway Remodeling

机译：抗IL-5受体α的单克隆抗体，但非IL-5抑制与气道重塑相关的气道高反应性

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Objective: A central role for eosinophils in the pathogenesis of asthma was recently nullified when it was shown that treatment with anti-IL-5 monoclonal antibody (mAb), mepolizumab, did not affect post-allergen airway hyperresponsiveness (AHR) in mild asthmatics. We hypothesized that the reason was airway remodeling.Design: We evaluated the effects of anti-IL-5 and anti-IL-5 receptor alpha (IL-5Ralpha) mAbs in murine asthma models with and without remodeling.Materials and Methods: BALB/c mice were immunized with ovalbumin adsorbed to alum at days 0 and 5. The mice without remodeling received inhaled ovalbumin at day 17, while the mice with remodeling received inhaled ovalbumin daily from days 17 to 30. Then, anti-IL-5 mAb or anti-IL-5Ralpha mAb was given 24 hours before challenge, and AHR were measured 24 hours after challenge. Also, IL-5Ralpha expression in human airway smooth muscle cells (ASMCs) was measured by immunocytochem-istry. The effect of IL-5 on human ASMCs growth and its inhibition by the mAb were determined.Results: Both anti-IL-5 mAb and anti-IL-5R# mAb inhibited airway eosinophilia and AHR in the mice without remodeling. In the remodeling model, anti-IL-5 mAb suppressed airway eosinophilia but not AHR. However, anti-IL-5Ralpha mAb inhibited both airway eosinophilia and AHR. Expression of IL-5Ralpha and growth were stimulated by IL-5 in human ASMCs; and the growth was inhibited by pretreatment with anti-IL-5Ralpha mAb, but not anti-IL-5 mAb.Conclusion: These results suggest that AHR is caused by IL-5 signaling via expression of IL-5Ralpha in human ASMCs, and airway remodeling is more important than inflammation. Monoclonal antibody against IL-5Ralpha, but not IL-5, can inhibit AHR in asthma with remodeling.
机译：目的：最近发现，嗜酸性粒细胞在哮喘发病机理中的重要作用被取消，因为它表明抗IL-5单克隆抗体（mAb）美泊珠单抗治疗不会影响轻度哮喘患者的变应原后气道高反应性（AHR）。我们假设其原因是气道重塑。设计：我们评估了有和没有重塑的小鼠哮喘模型中抗IL-5和抗IL-5受体α（IL-5Ralpha）mAb的作用。材料与方法：BALB / c小鼠在第0天和第5天用吸附在明矾上的卵白蛋白免疫。未重塑的小鼠在第17天接受吸入的卵白蛋白，而重塑的小鼠在第17天至30天每天接受吸入的卵白蛋白。然后，抗IL-5 mAb或在攻击前24小时给予抗IL-5RαmAb，并在攻击后24小时测量AHR。另外，通过免疫细胞化学法测量人气道平滑肌细胞（ASMC）中的IL-5Rα表达。结果：抗IL-5 mAb和抗IL-5R＃mAb均能抑制小鼠气道嗜酸性粒细胞增多和AHR，而不会重塑IL-5对人ASMC生长的抑制作用。在重塑模型中，抗IL-5 mAb抑制气道嗜酸性粒细胞增多，但不能抑制AHR。但是，抗IL-5Ralpha mAb抑制气道嗜酸性粒细胞增多和AHR。 IL-5在人ASMC中刺激IL-5Rα的表达和生长。结论：这些结果表明，AHR是通过人ASMCs和气道中IL-5Ralpha的表达通过IL-5信号传导引起的，它是由IL-5信号引起的。重塑比炎症更重要。抗IL-5Ralpha的单克隆抗体可抑制哮喘中的AHR，但不能抗IL-5。

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