Mechanism on Enhancing effect of chlorinated organic solvents as groundwater pollutants on Type I Allergy
Mechanism on Enhancing effect of chlorinated organic solvents as groundwater pollutants on Type I Allergy
批准号:
15590111
负责人:
NAGASE Hisamitu
金额:
$2.18万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2003
资助国家:
日本
项目状态:
已结题
起止时间:
2003 至 2004
中文摘要
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英文摘要
The prevalence rate of allergic diseases such as bronchial asthma and rhinitis is increasing in industrial areas and countries. There are some reports on epidemiological studies that may suggest a link between the incidence of allergic disease and environmental pollutants, such as diesel exhaust particles (DEPs), formaldehyde and volatile organic compounds (VOC). Chlorinated organic solvents are classified into VOC, and recently have become major environmental pollutants. Previously we observed the enhancing effects of some chlorinated organic solvents, such as tetrachloroethylene (PCE) and trichloroethylene (TCE), on histamine release from rat mast cells in vitro. In the present study, we investigated the enhancing effect of low concentration of PCE and TC dissolved in drinking water on Wistar rat. The chlorinated organic solvents enhanced passive cutaneous anaphylaxis (PCA) in a dose-dependent manner. Rat mast cell RBL-2H3 were incubated with anti-dinitrophenol (DNP) monoclonal IgE antibody, and then stimulated by DNP-BSA in the presence of PCE (0.01, 0.1 and 1 mg/L) or TCE (0.03, 0.3 and 3 mg/L). The conditioned medium and cell lysate were collected, and measured IL-4, TNF-α and MCP-1 by ELISA. Each inflammatory mediator production was increased in a dose-dependent manner. Furthermore, mRNA expression of them was evaluated by semi-quantitative RT-PCR, these mRNA expressions were found to be up-regulated by the exposure of PCE and TCE. Thus, this overexpression of inflammatory mediator from RBL-2H3 exposed to PCE and TCE is associated with inflammatory response in late phase. These results suggest that PCE and TCE, even in a low concentration, may affect the immune response via the modulation of cytokine production in mast cells, and lead to the augmentation of allergic diseases.
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