Project/Area Number |
16616007
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
アレルギー
|
Research Institution | Tohoku Pharmaceutical University |
Principal Investigator |
OHNO Isao Tohoku Pharmaceutical University, Pharmaceutical Sciences, Professor, 薬学部, 教授 (00250762)
|
Co-Investigator(Kenkyū-buntansha) |
SAKURADA Shinobu Tohoku Pharmaceutical University, Pharmaceutical Sciences, Professor, 薬学部, 教授 (30075816)
SATOH Naoko Tohoku Pharmaceutical University, Pharmaceutical Sciences, Associate Professor, 薬学部, 講師 (20364408)
SORA Ichirou Tohoku University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (40322713)
TAMURA Gen Tohoku University Hospital, Respiratory & Infectious Diseases, Associate Professor, 感染症呼吸器内科, 講師 (70188431)
|
Project Period (FY) |
2004 – 2005
|
Project Status |
Completed (Fiscal Year 2005)
|
Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2004: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
Keywords | allergy / bronchial asthma / stress / opioid / μ-oploid receptor / Th2 cytokine / オピイド / オピオイド受容体 / μ受容体 |
Research Abstract |
1.The effects of acute stress on allergic responses in asthma (1)Allergen-induced airway inflammation, in terms of the numbers of inflammatory cells in lung lavage fluids, in both restrain stressed-C57BL/6 and Balb/C female mice during allergen inhalation (acute stress) was significantly weaker than that in non restrain stressed-mice. (2)This effect of acute stress on the airway inflammation was observed also in μ opioid receptor-defficient C57BL/6 female mice. 2.The effects of chronic stress on allergic responses in asthma (1)Following restrain stress during allergen inhalation, mice were further loaded with the stress once a day for 6 consecutive days (chronic stress). After the last stress, mice were inhaled with allergen, and lung lavage fluids were collected. (2)The numbers of inflammatory cells and the contents of Th2 cytokine including IL-4, IL-5 and IL-13 in lung lavage fluids in chronic stressed- C57BL/6 female mice were significantly higher than those in non chronic stressed-mice. (3)The increase of inflammatory cell numbers in chronic stressed-mice was abolished by the simultaneous administration of a μ opiois receptor antagonist β-FNA, with the stress. (4)In μ opioid receptor-defficient C57BL/6 female mice, the numbers of inflammatory cells and the contents of Th2 cytokine in lung lavage fluids were not significantly different between with and without chronic stress. These results suggest, that acute and chronic stress have opposite effects, the improvement and exacerbation, respectively, on allergen-induced airway inflammation. that the effect of chronic stress, but not acute stress, was mediated, at least in part, by μ opioid receptors, and that one of the mechanisms underlying the exacerbation by chronic stress is the shift of immune responses to Th2 through the activation of μ opioid receptors. We are attempting to investigate the role of μ opioid receptors on hypothalamus-pituitary-adrenal axis and on T lymphocytes in the immune deviation.
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