| Project/Area Number |
18604005
|
|---|
| 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 | Kagawa University |
|---|
Principal Investigator |
KATOH Shigeki Kagawa University, Department of Cell Regulation, Associate Professor (10295206)
|
|---|
| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥4,050,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥450,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
|
|---|
| Keywords | Asthma / Allergy / Immunology / Cell adhesion molecule / CD44 / VLA-4 |
|---|
| Research Abstract |
Background: CD44 is a cell adhesion molecule that participates in lymphocyte adhesion to inflamed endothelium. CD44 hyaluronan interaction can promote extravasation and egress of antigen-activated lymphocytes on inflamed vascular beds. We recently found that anti-CD44mAb treatment inhibits the development of antigen-induced airway inflammation and airway hyperresponsiveness (AHR). In this study, we evaluated the effect of anti-CD44mAb on allergic airway inflammation in am〓e allergen-induced asthma model.
Methods: BALB/c mice were sensitized by intraperitoneal injections of Dermatophagoides faire allergen (Der) with alum on Days 0 and 14, and were challenged by intranasal administration of Der on Day 29. AHR to aerosolized methacholine was evaluated and bronchoalveolar lavage (BAL) was performed 24 hours after the antigen challenge.
Results: Anti-CD44mAb was administered intraperitoneally 12 hairs before intranasal antigen challenge. Administration of anti-CD44mAb significantly suppressed numbers of lymphocytes and eosinophils in BAL fluid (BALF) and inhibited AHR. Increases in IL-5 and IL-13 levels in BALF after the transnasal antigen administration were suppressed by anti-CD44mAb. Anti-CD44mAb inhibited the infiltration of peripheral blood Th2 cells into the airway. Anti-CD44mAb treatment of Derf-challenged mice did not influence total or Der-specific serum IgE levels.
Conclusion: Art-CD44mAb treatment reduced allergic airway inflammation and AHR by preventing lymphocytes (Th2 cells) and eosinophil accumulation in the lung. Thus, CD44 may be critical for development of allergic asthma.
|
