Project/Area Number |
07407072
|
Research Category |
Grant-in-Aid for Scientific Research (A)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
|
Research Institution | University of Tokyo |
Principal Investigator |
ITO Koji UNIVERSITY of Tokyo, Dpt. of Med. dPhys. Therap. Professor, 医学部・附属病院, 教授 (10008310)
|
Co-Investigator(Kenkyū-buntansha) |
SHOJI Shunsuke UNIVERSITY of Tokyo, Dpt. of Med. dPhys. Therap. Assistant Professor, 医学部・附属病院, 助手 (10171018)
TAKIZAWA Hajime UNIVERSITY of Tokyo, Dpt. of Med. dPhys. Therap. Assistant Professor, 医学部・附属病院, 助手 (80171578)
SUKO Matsunobu UNIVERSITY of Tokyo, Dpt. of Med. dPhys. Therap. Lecturer, 医学部・附属病院, 講師 (80107622)
OKUDAIRA Hirokazu UNIVERSITY of Tokyo, Dpt. of Med. dPhys. Therap. Lecturer, 医学部・附属病院, 講師 (30106645)
MORITA Yutaka UNIVERSITY of Tokyo, Dpt. of Med. dPhys. Therap. Associate Professor, 医学部・附属病院, 助教授 (60107620)
|
Project Period (FY) |
1995 – 1996
|
Project Status |
Completed (Fiscal Year 1996)
|
Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1996: ¥3,300,000 (Direct Cost: ¥3,300,000)
|
Keywords | Brochial Asthma / Airway Epithelium / T Cells / Mast Cells / Eosinophils / Cytokine Network / Repair / Remodeling / 気管支上皮細胞 / サイトカイン / フィブロネクチン / 接着因子 |
Research Abstract |
Bronchial asthma is characterized by profound bronchoconstriction and persistent airway inflammation associated with hyperresponsiveness. There is a dense accumulation of eosinophils, mast cells and lymphocytes, whcih are belived to play important roles in the pathogenesis of asthma. We investigated the cell-to-cell interactions, especially between airway epithelial cells and the inflammatory cells in vitro. Airway epithelial cell-derived fibronectin, IL-8 and RANTES showed a chemotactic activity for mast cells, Iymphocytes and eosinophils, respectively. Airway epithelial cells also express and release IL-6 and GM-CSF which activate lymphocytes and eosinophils, and epithelium-derived endothelin-lshowed a potent bronchoconstricting action on airway smooth muscles.We further showed that eosinophil adhesion to bronchial epithelial cells is one of the important signals for eosinophil activation and degranulation.Airway epithelial cell growth and differentiation are crucial steps for the repair processes of airway mucosa, and failure of correct repair may result in tissue remodeling. We demonstrated that both eosinophils and epithelial cells express TGFbeta, whcih may be a factor to suppress normal repair and to induce remodeling in the airways. We believe our findings gave new insights into the cell-to-cell interactions important in the thogenesis of asthma, and may help develop better strategies for the treatment of this disease.
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