| Project/Area Number |
62570341
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | Gunma University |
|---|
Principal Investigator |
NAKAZAWA Tsugio Professor. College of Medical Care and Technology Gunma University, 医療技術短期大学部, 教授 (70008316)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NAKAZAWA Tsugio Professor. College of Medical Care and Technology Gunma University (00110502)
|
|---|
| Project Period (FY) |
1988
|
| Project Status |
Completed (Fiscal Year 1988)
|
| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1988: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1987: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
|---|
| Keywords | Lipocortin / phospholipase A2 / LAR(late asthmatic responses) / LAR(遅発性喘息反応) / 遅発性喘息 / モルモット気管らせん法 |
|---|
| Research Abstract |
Lipoxortin is a phospholipase A2 inhibitory protein who mimics the antiinflammatory actions of glucocorticoids. LAR(late asthmatic responses) occurring several hours after allergen inhalation are important asthma and similar to severe-type asthma which often resists to the therapy. Corticosteroids may be related to the pathogenesis of LAR because prior administration of the steroids inhibits the development of LAR, and because low cortisol levels in the peripheral blood appears during LAR. The aim of this study is to search whether lipocortin contributes to the LAR development.
6 Mg of lipocortin fraction who had anti-phospholipase A2 activity, was isolated from human placenta and purified by gel filtration and DE column chromatography. However, changes of lipocortin during LAR could not be detected because a monoclonal antibody was not obtained from the hybridoma made by lipocortin immunized lymphocytes and myeloma cells of mice. Lipocortin partly suppressed the appearance of LAR in guinea pigs. It also inhibited the increased hyperresponsiveness of airways in guinea pigs who were in low cortisol levels after metopiron treatment.
These results suggest that a low level of lipocortin in the peripheral blood might be involved in the LAR development, and that LAR might appear as a results of phospholipase A2-induced inflammation.
|
