1997 Fiscal Year Final Research Report Summary
Experimental Study on a new mechanism of allergic asthma-like-pathogenesis.
| Project/Area Number |
08457143
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Public health/Health science
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| Research Institution | National Institute for Environmental Studies. |
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Principal Investigator |
SAGAI Masaru National Institute for Environmental Studies, Res.Team for Health Effects of Air Pollutants., Head of Res.Team., 地域環境研究グループ, 総合研究官 (80124345)
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| Co-Investigator(Kenkyū-buntansha) |
TAKANO Hirohisa National Institute for Environmental Studies, Res.Team for Health Effects of Air, 地域環境研究グループ, 主任研究員 (60281698)
ICHINOSE Takamichi National Institute for Environmental Studies, Res.Team for Health Effects of Air, 地域環境研究グループ, 主任研究員 (50124334)
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| Project Period (FY) |
1996 – 1997
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| Keywords | asthma / diesel exhaust particles / Diesel exhaust / Eosinophil infiltration / globlet cells / airway hyperresponsiveness / IgG1 antibody / IgE antibody |
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| Research Abstract |
We previously reported that there is a new mechanism of asthma-like pathogenesis via IgG1 antibody. To confirm this evidence, in the last year, we had compared the differences on expression of asthma-like-features such as 1) an infiltration of eosinophils into airway mucosa, 2) proliferation of goblet cells and 3) airway hyperresponsiveness by intratracheal instillation of diesel exhaust particles (DEP) and ovalbumin (OA) between BALB/c mouse with high ability of IgE production and C3H/He mouse with high ability of IgG1 production. We found that only C3H/He mouse had expressed astuma-like-features. This suggest that IgG1 antibody may play an important role on the expression of asthma-like-features.
In this year, we had carried out two experiments by intratracheal instillation of DEP and OA,and inhalation of diesel exhaust (DE) and OA to CH3/He mouse. In these exPeriment, first, OA+alum were administered intraperitoneally one time. Mice in DEP+OA group showed marked changes on the three features compared with the mice in OA group. IgE and IgG1 titers in the DEP+OA group were 2.2+0.8 and 47,000+6,400, respectively. Mice inhaled DE and OA also showed marked changes on the three features. However, the degree of the change was slightly moderate to compare with that in the mice administered DEP+OA.Although IgG1 titers were not different between DEP+OA and DE+OA groups, IgE titer in DE+OA group increased 15 times to compare with IgE titer in the DE+OA group.
From these results, there is no denying the involvement of IgE on the onset of asthma-like-features, because usage of alum is not suitable to make clear the involvement of only IgG1 antibody. Now, we reexamine an experiment without usage of alum on onset of asthma-like-features by inhalation of DE+OA.
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Research Products
(11 results)
