| Project/Area Number |
08670679
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | Teikyo University School of Medicine |
|---|
Principal Investigator |
OHTA Ken Department of Medicine Teikyo University School of Medicine Professor, 医学部, 教授 (30160500)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NAKAJIMA Miko Teikyo University School of Medicine, assistant Professor, 医学部, 助手 (10256034)
NAKANO Jyunichi Teikyo University School of Medicine, Associate Professor, 医学部, 講師 (20240707)
山田 和人 帝京大学, 医学部, 助手 (40240006)
|
|---|
| Project Period (FY) |
1996 – 1997
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
|---|
| Keywords | Asthma / Bronchial epithelial cells / GM-CSF / Immunogloblin / mouse / Allergen sensitization / Airway hyperresponsivenss / Anti-GM-CSF antibody / 気道過敏症 / 抗GM-CSF体 |
|---|
| Research Abstract |
It has been known that allergic inflammation at the airway and associated disorder of airway epithelial cells play important roles as causative factors for the airway hyperresponsiveness. In the study, we have studied cytokine production of bronchial epithelial cells in vitro and the effects of these cytokine in vivo to analyze mechanism of relationship between allergic inflammation and airway hyperresponsiveness. We used BEAS-2B cells, a cell line of bronchial epithelial cells transformed by adenovirus-12/SV-40 hybrid and cultured in F-12 medium. SIgA and anti IgA complex induced the release of GM-CSF and IL-8 in a dose-dependent manner. The existence of IgA receptor was demonstrated by flow cytometry analysis using anti-IgA receptor specific monoclonal antibodies. Next, we have established mice asthmatic model sensitized in ovalbumin specific manner and tried to clarify the effects of GM-CSF in vivo. A/J mice were first immunized with OA+Alum, following intranasal sensitization with QA.Intranasal sensitization with OA increased the airway responsiveness to acetylcholine. A pathological study revealed that the treatment with OA replaced the ciliated epithelial cells of the airways with Clara cells. The transnasal administration of GM-CSF neutralizing antibody completely inhibited the increase of airway hyperresponsiveness caused by OA.In conclusion, GM-CSF, which can be produced by bronchial epithelial cells, plays an important role in enhancing airway responsiveness at the site of the airway.
|
