| Project/Area Number |
14580572
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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 | Oita University of Nursing and Health Sciences |
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Principal Investigator |
ICHINOSE Takamichi Oita University of Nursing and Health Sciences, Department of Health Sciences, Professor, 看護学部・人間科学講座・生体反応, 教授 (50124334)
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| Co-Investigator(Kenkyū-buntansha) |
SADAKANE Kaori Oita University of Nursing and Health Sciences, Department of Health Sciences, Assistant, 助手 (20322381)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Asian dust / Bronchial astma / It injection / Murin Lung / Eosinophils / Goblet cells / IgE production / IgG1 production / アレルギー / 肺 / 毒性 / 炎症 / サイトカイン / ケモカイン / マウス / IL-5 / 気道炎症 / 抗体産生 |
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| Research Abstract |
Background: Asian sand dust (Kosa) contains irritant chemical species, such as SO^<2->_4. Although Kosa causes adverse respiratory health effects, there is no experimental study showing the effect of Kosa on allergic asthma. This study was undertaken to clarify the effects of Kosa on ovalbumin (OVA)-induced eosinophilic inflammation in the murine lung. Methods: ICR mice were administered intratracheally with saline; Kosa alone (sample from Shapotou desert); Kosa plus SO^<2->_4 (Kosa -SO_4); Natural Asian dust (NAD) from Beijing; OVA, OVA + Kosa; OVA + Kosa -SO_4; or OVA + NAD. Results: The three sand dusts, especially NAD, aggravated the eosinophilc airway inflammation accompanied by OVA-induced goblet cell proliferation. The additive effect of SO^<2->_4 was not observed. OVA which was induced by sand dusts suppressed the expression of interleukin (IL)-1 2 and interferon (IFN)-γ in bronchoalveolar lavage fluids (BALF). In contrast, these sand dusts, especially NAD, synergistically increased IL-5, eotaxin, and monocyte chemotactic protein (MCP)-1 in BALF and lung tissue related to OVA. NAD caused the adjuvant effects to IgG1 and IgE production. Conclusions: These results suggest that sand dusts enhance OVA-induced eosinophilic inflammation in the lungs. It is hypothesized that this enhancement is induced by the synergistic effect between IL-S and eotaxin and MCP-1 via the suppression of IL-12 and IFN-γ
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