Author/Authors :
Yamashita، نويسنده , , Naomi and Tashimo، نويسنده , , Hiroyuki and Ishida، نويسنده , , Hirofuni and Matsuo، نويسنده , , Yukiko and Arai، نويسنده , , Hidenori and Nagase، نويسنده , , Hiroyuki and Adachi، نويسنده , , Tetsuya and Ohta، نويسنده , , Ken، نويسنده ,
Abstract :
Insulin-like growth factor (IGF)-I is known to act on fibroblasts as a progression factor to push cells toward proliferation and activation to synthesize collagen. Subepithelial fibrosis, collagen deposition at the lamina reticularis, is part of the process of so-called remodeling and is a characteristic finding in the asthmatic airway. To study the role of IGF in the evolution of asthma, we used a model that involved immunization of mice with ovalbumin and alum, followed by an inhaled challenge of ovalbumin. IGF-I neutralizing antibody was continuously infused with an osmotic pump. Pulmonary function was analyzed using whole-body plethysmography before and after acetylcholine administration. It was found that OVA inhalation induced IGF-I expression at the site of the airway. IGF-I neutralizing Ab inhibited the elevation of airway resistance, airway inflammation, and an increase in airway wall thickening. The depression of ICAM-1 expression was accompanied by a diminution in airway inflammation. In conclusion, these results suggest that IGF-I is likely to be an important mediator of inflammation and remodeling in the asthmatic airway.
Keywords :
allergy , cytokines , inflammation , Adhesion Molecules