Kidins220/ARMS contributes to airway inflammation and hyper-responsiveness in OVA-sensitized mice.

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.