1998 Fiscal Year Final Research Report Summary
Intercellular action between human lung mast cells and eosinophils
| Project/Area Number |
09670465
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内科学一般
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| Research Institution | Gunma University |
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Principal Investigator |
KANAZAWA Tsugio Gunma University, School of Health Sciences, 医学部・保健学科, 教授 (70008316)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Human lung mast cell / eosinophil / IL-3 / IL-5 / TNF-alpha(tumor necrosis factor alpha) / GM-CSF(granulocyte-macrophage colony stimulating factor) |
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| Research Abstract |
Recent works suggest that network of intercellular reactions among inflammatory cells including lymphocytes, mast cells and eosinophils contribute to production of chronic allergic inflammation. Aim of this study is to search intercellular action between mast cell and eosinophils in human lung. By using RT-PCA, in site hybridization, enzyme immunoassay and immunocytometry, we studied the production of GM-CSF(granulocyte-macrophage colony stimulating factor), IL-3, IL-5 and TNF- alpha (tumor necrosis factor alpha) in human lung mast cells and the localization of mRNA of these cytokines, and studied their effect to eosinophils.
Purified human lung mast cells challenged with anti-IgE produced inflammatory cytokines such as GM-CSF,IL-3, IL-5 and TNF- alpha protein 4-8 hours after the activation. The mast cells supernatant induced ECP(eosinophil cationic protein) release from eosinophils and the release was significantly inhibited by blocking monoclonal antibodies against GM-CSF, IL-5, and TNF- alpha.
Corticosteroid (beta methasone) suppressed dose-dependently suppressed the release of GM-CSF from human lung mast cells. TNF- alpha was produced by stimulation of substance P.It suggests that the cytokine is also released by non-IgE stimulation.
These findings indicate that human mast cells are an important cellular source of various cytokines and may contribute to chronic eosinophil-mediated inflammation.
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