| Project/Area Number |
26461469
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Nippon Medical School (2015-2016)
Yokohama City University (2014) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
桐野 洋平 横浜市立大学, 医学部, 講師 (50468154)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ベーチェット病 / M1マクロファージ / M2マクロファージ / IL-10 / CCR2 / CCR1 / HO-1 / CD163 |
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| Outline of Final Research Achievements |
This study aimed to show a critical role of defective anti-inflammatory M2 macrophage function in Behcet’s disease (BD), because previous studies have shown that defective heme oxygenase-1 (HO-1) expression and IL-10 production are involved in BD. We established in vitro M1 and M2 differentiation systems using GM-CSF and M-CSF, respectively. M2 cells preferentially expressed CCR1, which is also functionally impaired in BD, in addition to HO-1 and IL-10, and migrated more sensitively to MIP-1a than M1 cells. These data suggest that M2 macrophage dysfunction is implicated in development of BD inflammation. Furthermore, in vitro induced M1 cells acquired capacity of IL-10 production in presence of M-CSF, indicating the functional plasicity of macrophages. This findings suggested that phenotypic conversion of macrophages is a promising therapeutic strategy for BD.
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