1997 Fiscal Year Final Research Report Summary
AIRWAY MUCOSA CELLS PRODUCE CHEMOTACTIC FACTOR(S) FOR MAST CELLS.
Project/Area Number |
08670657
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
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Research Institution | The UNIVERSITY OF TOKYO |
Principal Investigator |
SHOJI Shunsuke UNIVERSITY OF TOKYO HOSPITAL, ASSISTANT PROFESSOR, 医学部・附属病院, 助手 (10171018)
|
Co-Investigator(Kenkyū-buntansha) |
HONDA Zen-ichiro UNIVERSITY OF TOKYO HOSPITAL, LECTURER, 医学部・附属病院, 講師 (70238814)
|
Project Period (FY) |
1996 – 1997
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Keywords | CHEMOTAXIS / MAST CELLS / AIRWAY MUCOSA / FIBROBLASTS / VASCULAR ENDOTHELIAL CELLS |
Research Abstract |
In the allergic diseases, including bronchial asthma, the airway mast cells in the bronchial mucosa may contribute to the pathogenesis of such diseases by releasing a variety of mediators and cytokines. Although the relation between airway mast cells and the peribronchial fibrosis have recently been highlighted, it is not known which types of cells in the airway mucosa are capable of releasing chemotactic factor(s) for those mast cells. In the present study, we cultured bronchial epithelial cells, fibroblasts and vascular endothelial cells in vitro, and assayed for the chemotactic activity in the culture supernatant conditioned media of those cells. The results demonstrated that bronchial epithelial cells, fibroblasts and vascular endothelial cells can release chemotactic activity for mast cells, and one of the potent chemotactic factor derived from epithelial cells was identified as fibronectin. In addition, it was certified that the fibronectin-directed mast cell chemotaxis could be controlled by the Src family tyrosine kinase, Lyn, during the intracellular signal transduction. It will be the future problem how we should manage for the mast cell chemotaxis in the allergic airway disease such as bronchial asthma.
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