1997 Fiscal Year Final Research Report Summary
Role of 1ymphocytes in airway inflammation and hyperresponsiveness induced by diesel exhaust particles.
| Project/Area Number |
08680591
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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 |
環境影響評価(含放射線生物学)
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| Research Institution | National Institute For Environmental Studies |
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Principal Investigator |
TAKANO Hirohisa National Institute For Environmental Studies, Regional Environment Division, Senior Researcher, 地域環境研究グループ, 主任研究員 (60281698)
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| Project Period (FY) |
1996 – 1997
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| Keywords | dicsel exhieus particles / brenchial asthma / eosinophilic airway inflimmation / lymphocytos / cytokine / interleukin-5 / surfoce markers |
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| Research Abstract |
Previous experimental studies have suggested that nasal instillation of diesel exhaust particles (DEP) can enhance nasal lgE response and cytokine production ; However, there is no experimental evidence for the relation of DEP to allergic asthma. We investigated the effects of DEP inoculated intratracheally on antigen-induced airway inflammation, local expression of cytokine proteins, and antigen-specific immunoglobulin production in mice. DEP aggravated ovalbumin-induced airway inflammation characterized by infiltration of eosinophils and lymphocytes and an increase in goblet cells in bronchial epithelium. DEP with antigen markedly increased interleukin. 5 (lL-5) protein levels in lung tissue and bronchoalveolar lavage supernatants compared with either antigen or DEP alone. The combination of DEP and antigen induced significant increases in local expression of IL-4, granulocyte macrophage-colony stimulating factor (GM-CSF), and IL-2, whereas expression of interferon-gamma was not affected. In addition, DEP exhibited adjuvant activity for the antigen-specific production of lgG and lgE.These results provide the first experimental evidence that DEP can enhance the manifestations of allergic asthma. The enhancement may be mediated mainly by the increased local expression of IL-5, and also by the modulated expression of lL-4, GM-CSF,and lL-2.
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