2001 Fiscal Year Final Research Report Summary
The mechanism of development of nasal hypersensitivity: Role of T cell and approach to treatment
| Project/Area Number |
12671657
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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 |
Otorhinolaryngology
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| Research Institution | Yamanashi Medical University |
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Principal Investigator |
MATSUZAKI Zensei Yamanashi Medical University, Department of otorlaryngology, Assistant professor, 医学部, 講師 (90283217)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Yoshitaka Yamanashi Medical University, epartment of otorlaryngology, Professor, 医学部, 教授 (40169157)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Nasal allergy / Nasal hypersensitivity / Eosinophil infiltration / Mast cell / CD4+T cell / cell transfer / Th l / Th2 / RS virus infection |
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| Research Abstract |
The influence of T cell on the development of nasal hypersensitivity was studied.The nasal hypersensitivity against histamine and increased number of eosinophils infiltrated in the nasal mucosa was observed in the mice lacking lacking CD4+T cells or in the mice lacking mast cells, both of which had been transferred Th2 rich CD4+T cells of ovalbumin sensitized mice. The transfer of Thl cells specific for ovalbumin to ovalbumin sensitized mice also did not improve the nasal hypersensitivity. Thus, eosinophils and mast cell seem to be not always necessary for the induction of nasal hypersensitivity and Th2 cytokines but not Thl cytokine may be strongly involved for the induction.
In additional study, acute RSV infection enhances response to subsequent sensitization to ovalbumin and also strongly enhance the sensitivity of former sensitized mice. The production of Th2 cytokines, not only of Thl cytokines in these infected mice seems to be associated with the development of nasal hypersensitivity. However, in the study with IL-10 transgenic (TG) mice, which expressed a large amount of IL-10 in the nasal mucosa, viral replication in the respiratory tract after intranasal infection with RSV was significantly suppressed compared to those in non-TG mice. Although IL-10 is one of Th2 type cytokines and is known to have an anti-inflammatory function, IL-10 may contribute to the anti-viral defense and to reduction of nasal hypersensitivity under these condition. Thus, a variety of mechanisms may contribute to the development of nasal hypersensitivity and hyperresponsiveness induced by T cells.
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