Department of Neurobiology, Institute of Respirotory Diseases, China Medical University, Shenyang 110001, China.
Respir Physiol Neurobiol. 2011 Jan 31;175(1):97-103. doi: 10.1016/j.resp.2010.09.012. Epub 2010 Sep 24.
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-1β, IL-4 and TNF-α were determined by ELISA, and NF-κB activation determined by EMSA. Kidins220/ARMS expression was observed in ovalbumin-sensitized mice by immunofluorescence or western blotting. IL-1β, IL-4, and TNF-α were overexpressed and NF-κB activation increased after allergen challenge compared with controls. After treatment with anti-ARMS or anti-NGF, levels of IL-1β, IL-4 and TNF-α and NF-κB 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.
BALB/c 小鼠用卵清蛋白致敏和激发，我们假设 Kidins220/ARMS 在变应原性气道挑战期间影响气道炎症和高反应性，并通过向小鼠鼻腔内给予抗神经生长因子抗体或抗 ARMS 抗体来评估。使用密封整体肺活量计测量气道阻力。通过 ELISA 测定 BALF 中总细胞数和不同炎性细胞的百分比，通过 EMSA 测定 NF-κB 激活。通过免疫荧光或蛋白质印迹观察卵清蛋白致敏小鼠中的 Kidins220/ARMS 表达。与对照组相比，过敏原激发后 IL-1β、IL-4 和 TNF-α 过度表达，NF-κB 激活增加。与卵清蛋白致敏小鼠相比，用抗 ARMS 或抗神经生长因子治疗后，IL-1β、IL-4 和 TNF-α 水平以及 NF-κB 激活降低。这些结果表明，NGF 介导的 Kidins220/ARMS 信号参与哮喘的发病机制，并有助于卵清蛋白致敏小鼠的气道炎症和高反应性。
