2003 Fiscal Year Final Research Report Summary
Approaches to the pathogenesis of bronchial asthma
| Project/Area Number |
13670603
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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 | HIROSHIMA UNIVERSIlY (2003)
Ehime University (2001-2002) |
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Principal Investigator |
YOKOYAMA Akihito Hiroshima University, Graduate School of Biomedical Sciences, Assistant Professor, 大学院・医歯薬学総合研究科, 講師 (30191513)
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| Co-Investigator(Kenkyū-buntansha) |
KOHNO Nobuyuki Hiroshima University, Graduate School of Biomedical Sciences, Professor, 大学院・医歯薬学総合研究科, 教授 (80215194)
NAKA Tetsuji Osaka University, Faculty of Medicine, Research associate, 医学部, 助手 (30303936)
HAMADA Hironobu Ehime University, School of Medicine, Research associate, 医学部・附属病院, 助手 (80314954)
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| Project Period (FY) |
2001 – 2003
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| Keywords | cytokine / bronchial asthma / eosinophil / interleukin |
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| Research Abstract |
Expression of SOCS family mRNA was examined in lung and spleen in a mouse model of asthma. Augmented expression of SOCS-1 but not SOCS-3 and SOCS-5 was observed in the lung. The expression of SOCS-1 was peaked in the first challenge, when maximum expressions of IL-4 and IFN-g mRNA were observed. The SOCS mRNA expressions were not changed in the spleen. To explore the role of SOCS-1, we examined the effects of exogenous administration of SOCS-1/liposome to the asthma model. The eosinophilic inflammation was significantly diminished following SOCS-1/liposome in comparison with null/liposome administration. Furthermore, prolonged eosinophilic inflammation was observed in an asthma model in SOCS-1^<+/-> mice. These results indicated that SOCS-1 is involved in eosinophilic airway inflammation, and it could promote resolution. of the inflammation.
We originally observed IL-12 inhibitory factor in the supernatants from antigen-stimulated splenic T cells obtained from asthma model mice. The estimated molecular weight of inhibitory factor was almost equal to naive mouse IL-10 by HPLC. Since the inhibitory activity was neutralized by addition of anti-IL-10 antibody, we concluded that the factor is IL-10. This means IL-10. is the most important for diminishing IL-12 in mouse model of asthma.
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