2003 Fiscal Year Final Research Report Summary
New pathogenesis and therapeutic : strategy for diffuse panbronchiolitis by regulation of intracellular apoptotic molecules
| Project/Area Number |
13670605
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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 | Oita University |
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Principal Investigator |
KADOTA Jun-ichi Oita University, Faculty of Medicine, Associate Professor, 助教授 (50233838)
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| Co-Investigator(Kenkyū-buntansha) |
KOHNO Shigeru Nagasaki University, School of Medicine, Professor, 大学院・医学研究科, 教授 (80136647)
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| Project Period (FY) |
2001 – 2003
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| Keywords | diffuse panbronchiolitis / apoptosis / Bax / Bcl-2 / caspase / macrolide antibiotics / Pseudomonas aeruginosa / biofilm |
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| Research Abstract |
1)No immunostain of Bax was observed in lymphocytes around respiratory bronchioles of diffuse panbronchiolitis (DPB), while Bcl-2 was stained in the majority of the lymphocytes. Furthermore, apoptosis-inducing enzyme, caspase 3 was also unstained. This indicates that over expression of Bcl-2 protein plays an important role in suppression of lymphocyte apoptosis in DPB.
2)14- or 15-membered ring macrolide antibiotics at 100 mg/l induced apoptosis of CD3/CD28-activated lymphocytes obtained from healthy volunteers through downregulation of anti-apoptotic protein, Bcl-xL. This suggest that macrolides influence intracellular signal, especially anti-apoptotic protein.
3)In a murine model with chronic Pseudomonas aeruginosa infection, 80-day administration of 14-membered macrolide antibiotic, erythromycin inhibited the biofilm formation of P.aeruginosa followed by elimination of the bacteria. This is a first report, indicating in vivo that long-term treatment of macrolides can eliminate the bacteria through destruction of biofilm formation.
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