インデックス付き
  • 学術雑誌データベース
  • Jゲートを開く
  • Genamics JournalSeek
  • アカデミックキー
  • ジャーナル目次
  • 中国国家知識基盤 (CNKI)
  • ウルリッヒの定期刊行物ディレクトリ
  • 電子ジャーナルライブラリ
  • レフシーク
  • ハムダード大学
  • エブスコ アリゾナ州
  • OCLC-WorldCat
  • SWBオンラインカタログ
  • 仮想生物学図書館 (vifabio)
  • パブロン
  • ジュネーブ医学教育研究財団
  • ユーロパブ
  • Google スカラー
このページをシェアする
ジャーナルチラシ
Flyer image

概要

Molecular Mechanisms of Metaplasia, Differentiation and Hyperplasia of Goblet Cellin Allergic Asthma

Toshiharu Hayashi

Bronchial allergic asthma (asthma) is an airway inflammation characterized by airflow obstruction of variable degrees with bronchial hyper-responsiveness and is induced by a complex interaction of environmental and genetic factors. Asthma of the human can be divided into an immediate- and a late-phase reaction, and some of the patients develop a late-phase reaction after a symptom-free interval. Hallmarks of asthma are mucus overproduction by goblet cells associated with responses of helper T(Th)2 cells. Mucus hypersecretion from goblet cells themselves or by metaplasia and/or hyperplasia of goblet cells appears to be associated with disease severity in asthma, because mucus production by those cells in local bronchial–bronchiolar lesions causes airway mucus plugging. However, the mechanisms of mucus production are not fully understood. Molecular mechanisms of goblet cell metaplasia, differentiation and hyperplasia will be reviewed in this article. Also, the relationship between allergic inflammation in Th1/Th2 paradigm shift and thymic stromal lymphopoietin (TSLP) was included for the understanding of goblet cell response in asthma. The clarification of mechanisms of mucin production in vivo may lead to the development of novel therapeutic strategies to suppress mucus production in asthma.