• Kohei Yamauchi.
• Third Department of Internal Medicine, Iwate Medical University School of Medicine, 19-1 Uchimaru, Morioka 020-8505, Japan. kyamauch@iwate-med.ac.jp
• Tohoku J. Exp. Med. 2006 Jun 1; 209 (2): 75-87.

AbstractBronchial asthma has been characterized by chronic and allergic airway inflammation, which induces cytological and histological changes in the airway structure over time. These changes have been called airway remodeling, which includes goblet cell hyperplasia, subepithelial fibrosis, and hyperplasia and hypertrophy of airway smooth muscle cells. Airway epithelium in asthma is often occupied with goblet cells, which contain secretory granules. Airway wall thickness increases because of subepithelial fibrosis, and hyperplasia and hypertrophy of airway smooth muscle cells and submucosal glands. Airway remodeling, therefore, can often cause irreversible airflow limitation, an increase of airway hyperresponsiveness and severity of asthma. Recent studies have demonstrated the molecular and cellular mechanisms of goblet cell hyperplasia, subepithelial fibrosis, and hyperplasia and hypertrophy of airway smooth muscle cells. Several lines of evidence suggest that airway remodeling has been induced by cytokines and mediators produced in chronic allergic airway inflammation. Thus, early intervention with inhaled corticosteroid may prevent progress of airway remodeling by suppressing allergic airway inflammation.

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