Kidins220/ARMS contributes to airway inflammation and hyper-responsiveness in OVA-sensitized mice
Kidins220/ARMS contributes to airway inflammation and hyper-responsiveness in OVA-sensitized mice
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Kidins220/ARMS 导致 OVA 致敏小鼠气道炎症和高反应性
DOI：
10.1016/j.resp.2010.09.012
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发表时间：
2011-01-31
影响因子：
2.3
通讯作者：
Liu, Yuli
中科院分区：
文献类型：
--
作者：
Ni, Xiuqin;Li, Xing;Liu, Yuli
用卵清蛋白致敏和激发BALB/c小鼠。我们假设Kidins220/ARMS在过敏性呼吸道攻击中影响呼吸道炎症和高反应性，并通过鼻腔注射抗NGF抗体或抗ARM抗体对小鼠进行评估。采用封闭式全身体积描记仪测量气道阻力。计数BALF中细胞总数和不同炎性细胞的百分比。用双抗体夹心法检测IL-1β、IL-4和肿瘤坏死因子-α的表达，用EMSA法检测核因子-kappaB的活化。免疫荧光法和免疫印迹法检测卵清蛋白致敏小鼠Kidins220/ARMS的表达。与对照组相比，过敏原攻击后IL-1β、IL-4和TNF-α高表达，核因子-kappaB活性增强。经抗ARM或抗NGF治疗后，IL-1β、IL-4、TNF-α水平及核因子-kappaB活性较卵蛋白致敏小鼠明显降低。这些结果表明，NGF介导的Kidins220/ARMS信号通路参与了哮喘的发病机制，并参与了卵蛋白致敏小鼠的呼吸道炎症和高反应性。(C)2010爱思唯尔B.V.保留所有权利。
BALB/c mice were sensitized and challenged with ovalbumin. We hypothesized that Kidins220/ARMS influences airway inflammation and hyper-responsiveness during allergic airway challenge, and assessed it by intranasal administration of anti-NGF antibody or anti-ARMS antibody to mice. Airway resistance was measured using a sealed whole-body plethysmograph. Total cell numbers and the percentage of different inflammatory cells in BALF were counted. Expression of IL-1 beta, IL-4 and TNF-alpha were determined by ELISA, and NF-kappa B activation determined by EMSA. Kidins220/ARMS expression was observed in ovalbumin-sensitized mice by immunofluorescence or western blotting. IL-1 beta, IL-4, and TNF-alpha were overexpressed and NF-kappa B activation increased after allergen challenge compared with controls. After treatment with anti-ARMS or anti-NGF, levels of IL-1 beta, IL-4 and TNF-alpha and NF-kappa B activation were reduced in comparison with those of ovalbumin-sensitized mice. These results suggest that NGF-mediated Kidins220/ARMS signaling participates in the pathogenesis of asthma, and contributes to airway inflammation and hyper-responsiveness in ovalbumin-sensitized mice. (C) 2010 Elsevier B.V. All rights reserved.