کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5926565 1167373 2011 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Kidins220/ARMS contributes to airway inflammation and hyper-responsiveness in OVA-sensitized mice
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی فیزیولوژی
پیش نمایش صفحه اول مقاله
Kidins220/ARMS contributes to airway inflammation and hyper-responsiveness in OVA-sensitized mice
چکیده انگلیسی

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.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Respiratory Physiology & Neurobiology - Volume 175, Issue 1, 31 January 2011, Pages 97-103
نویسندگان
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