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pubmed-article:16168397pubmed:abstractTextInsulin-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.lld:pubmed
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pubmed-article:16168397pubmed:articleTitleRole of insulin-like growth factor-I in allergen-induced airway inflammation and remodeling.lld:pubmed
pubmed-article:16168397pubmed:affiliationDepartment of Pharmacology, Research Institute of Pharmaceutical Sciences, Musashino University, Japan.lld:pubmed
pubmed-article:16168397pubmed:publicationTypeJournal Articlelld:pubmed
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