| Project/Area Number |
10670565
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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 |
Respiratory organ internal medicine
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| Research Institution | Nihon University |
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Principal Investigator |
HORIE Takashi Nihon University School of Medicine, First Department of Internal Medicine, Professor, 医学部, 教授 (60090081)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Shu Nihon University School of Medicine, First Department of Internal Medicine, Assistant Professor, 医学部, 講師 (30159090)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | exercise-induced asthma / hyperosmolarity / cooling / cytokine / airway epithelial cell / MAP kinase / 高侵透圧 / p38 MAPキナーぜ / 低温ストレス / 高浸透圧ストレス / p38マップキナーゼ |
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| Research Abstract |
We examined the basic mechanism in the recruitment of eosinophils and neutrophils into the airway of exercise-induced asthma. To clarify these issues, we exposed airway epithelial cells (AEC) to hyperosmolar medium and cold medium, and IL-8 and RNATES in the culture supernatants were determined. We simultaneously examined the role of p38 MARK and JNK in cytokine production in response to hyperosmolarity and cooling. The results showed that hyperosmorality and cooling induced p38 MAPK and JNK activation and that a specific inhibitor of p38 MAPK and a specific inhibitor of JNK inhibited IL-8 and RANTES production by AEC in response to hyperosmolarity, and cooling and rewarming, indicating that p38 MAPK and JNK regulate IL-8 and RANTES production by AEC upon the environmental stresses including hyperosmolarity and low temperature. Finally, we examined the effect of inhalant corticosteroids on cytokine production in response to hyperosmolarity and cooling/rewarming. Inhalant corticosteroids inhibited cytokine production. Although it is not known, at this time, whether inhaled corticosteroids are capable of producing beneficial effect in preventing development of a LPR induced by exercise, our results may indicate that a strategy of inhibiting IL-8 and RANTES production may apply to preventing development of a LPR induced by exercise as well as reducing the allergic inflammation of asthmatic airway. In conclusion, the present study supported by grant-in-aid for scientific research clarified the basic mechanism in airway inflammation which might be occurred in EIA and a potential beneficial effect of inhalant corticosteroids in preventing development of a LPR induced by exercise.
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