Experimental study on pathogenesis of asthma like symptom caused by combination of diesel exhaust and allergen.
Experimental study on pathogenesis of asthma like symptom caused by combination of diesel exhaust and allergen.
批准号:
10680528
负责人:
ICHINOSE Takamichi
金额:
$1.47万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1998
资助国家:
日本
项目状态:
已结题
起止时间:
1998 至 1999
中文摘要
我们通过长期暴露柴油机(DE)、Oalbumin(OA)治疗或两者结合,在空中考察了历史学的变化。航空上的历史学表现与免疫球蛋白生产或肺部局部细胞因子水平之间的关系也是研究的一部分。ICR mice were exposed to clean air or DE at a soot concentrations of 0. 3、1. 0 or 3. 0 mg/mイイD13イエD1 for 34 or 40 weeks。在15周后进行DE暴露,老鼠用10微克的OA敏感的内向剂,并在3周间隔后在最后18或24周的暴露中挑战1%OA的气溶胶。对DE进行34周的暴露,导致了典型变化的剂量依赖增加,如空气中的非硅化细胞增殖和表皮细胞增殖,但在空气中没有显示出goblet细胞增殖在血液中的表皮和碘氮素回收中的影响。OA挑战表明,在goblet cell proliferation和eosinophil recc中存在着非常明显的变化 ... More ruitment。OA和DE暴露的组合在3.0 mg/m D13 E D1产生的增加的改变的goblet cells和eosinophils,在DE中添加到进一步增加的类型变化的进一步增加。“暴露在3.0 mg/m的D13中的DE D1为40周的增强的过敏诱导的eosinophil recruitment into the submucos in the airways, and increased protein level of GM-CSF and IL-5 in the lungs。The increases in the eosinophil recruitment and the local cytokine expression were accompanied by those in goblet cell proliferation in the bronchial epithelium and airway hyperresponsiveness to inhaled acetylcholine。OA治疗在等离子体中产生了特定的OA IgG 1和IgE,当对DE暴露的免疫球蛋白生产的适当影响时没有观察到。目前的研究提供了一个实验证据,即DE的日常抑制可以增强这种过敏诱导的呼吸道疾病,如过敏性哮喘。这种影响可能主要由IL-5和GM-CSF增强的局部表达式介导。Less(低)
英文摘要
We investigated the histopahologic changes in the airway by long term exposure to diesel exhaust (DE), ovalbumin (OA) treatment or the both combination. The relation between the histopahologic appearances in the airway and immunoglobulin production or levels of local cytokines in the lungs was also studies. ICR mice were exposed to clean air or DE at a soot concentrations of 0.3, 1.0 or 3.0 mg/mィイD13ィエD1 for 34 or 40 weeks. Fifteen weeks after exposures to DE, mice were sensitized intraperitonealy with 10 μg of OA, and challenged aerosol of 1% OA at 3-week intervals during the last 18 or 24 weeks of the exposures. Exposure to DE for 34 weeks caused dose-dependent increases of the typical changes such as non-ciliated cell proliferation and epithelial cell hypertrophy in the airway, but showed no effect on goblet cell proliferation in the bronchial epithelium and eosinophil recruitment in the airway. OA challenge induced very alight changes in goblet cell proliferation and eosinophil rec … More ruitment. The combination of OA and DE exposure at 3.0 mg/mィイD13ィエD1 produced increased changes of goblet cells and eosinophils, in addition to further increases of the typical changes induced by DE. "Exposure to DE at 3.0 mg/mィイD13ィエD1 for 40 weeks also enhanced allergen-induced eosinophil recruitment into the submucos in the airways, and increased protein levels of GM-CSF and IL-5 in the lungs. The increases in the eosinophil recruitment and the local cytokine expression were accompanied by those in goblet cell proliferation in the bronchial epithelium and airway hyperresponsiveness to inhaled acetylcholine. OA treatment induced OA-specific IgG1 and IgE production in plasma, whereas the adjutant effects of DE exposure on the immunoglobulin production were not observed. The present study provides experimental evidence that daily inhalation of DE can enhance the allergen-induced respiratory disease such as allergic asthma. This effect may be mediated mainly by the enhanced local expression of IL-5 and GM-CSF. Less
期刊论文(3)
专著(0)
科研奖励(0)
会议论文
Takemichi Ichinose et al: "Long-term exposure todiesel exhaust enhances antigen-induced eossinophilic inflamation and epithelial damage in murin airway"Toxicological Sci. 44. 70-79 (1998)
Takemichi Ichinose 等人:“长期暴露于柴油尾气会增强鼠气道中抗原诱导的嗜酸性粒细胞炎症和上皮损伤”Toxicological Sci.
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通讯作者:
Takamichi Ichinose, Hirohisa Takano, Yuichi Miyabara and Masaru Sagai: "Long-term exposure to diesel exhaust enhances antigen-induced eoshinophilic inflammation and epithelia damage in murine airway"Toxicological Sci. 44. 70-79 (1998)
Takamichi Ichinose、Hirohisa Takano、Yuichi Miyabara 和 Masaru Sagai:“长期暴露于柴油废气会增强小鼠气道中抗原诱导的嗜酸性粒细胞炎症和上皮细胞损伤”毒理学科学。
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Takamichi Ichinose et al.: "Long-term exposure to diesel exhaust enhances antigen-induced eosinophilic inflammation and epithelial damage in murin airway"Toxicological Sci,. 44. 70-79 (1998)
Takamichi Ichinose 等人:“长期暴露于柴油机尾气会增强小鼠气道中抗原诱导的嗜酸性粒细胞炎症和上皮损伤”Toxicological Sci,.
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Detection of harmful airborne microbes transported across the China continent and evaluation of respiratory system effects by experimental research
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批准号:16H02969
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$11.4万
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财政年份:2016
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负责人:ICHINOSE Takamichi
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依托单位:
Effects of Asian sand dust on airway diseases and genetic susceptibility factors for exacerbation of allergic diseases
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批准号:22241011
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项目类别:Grant-in-Aid for Scientific Research (A)
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资助金额:$30.62万
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财政年份:2010
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负责人:ICHINOSE Takamichi
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依托单位:
Enhancement of Allergen-induced Eosinophilic Inflammation and Cytokine/Chemokine Expression Expression in the Murine Lungs by Asian Sand Dust
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批准号:14580572
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.79万
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财政年份:2002
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负责人:ICHINOSE Takamichi
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依托单位:
Murine strain differences in airway inflammation induced by diesel exhaust and house dust mite allergen
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批准号:12680550
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.73万
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财政年份:2000
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负责人:ICHINOSE Takamichi
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依托单位:
Experimental study on IgE non-dependent asthma like symptom and mice strain differences
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批准号:08680588
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.47万
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财政年份:1996
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负责人:ICHINOSE Takamichi
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依托单位:
海外基金