| Project/Area Number |
26461407
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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 |
Hematology
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| Research Institution | Kumamoto University |
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Principal Investigator |
Suzu Shinya 熊本大学, エイズ学研究センター, 教授 (80363513)
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| Co-Investigator(Renkei-kenkyūsha) |
Noyori Osamu 熊本大学, エイズ学研究センター/国際先端医学研究拠点施設, 特定事業研究員 (30737151)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 細胞分化 / マクロファージ / サイトカイン / IL-32 / 分化 / M-CSF |
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| Outline of Final Research Achievements |
M-CSF stimulates differentiation/survival of macrophages (MF) and induces anti-inflammatory M2 but not pro-inflammatory M1 MF. Recently, another cytokine IL-32 was reported to promote MF differentiation. Here, we found that M-CSF has additive/inhibitory effects on IL-32 activities. When added to M-CSF-MF, these cytokines supported MF survival, which was enhanced by their combination. However, they had opposed effects on HIV-1 replication; stimulated by M-CSF and inhibited by IL-32. Anti-HIV-1 activity of IL-32 was cancelled by M-CSF. Such effect of M-CSF was not seen with IL-32-induced M1-like features including high cytokine/chemokine production and CD80 expression. Of interest, IL-32-treated MF showed also M2-like features including high phagocytosis and expression of CD14 and CD163, the latter of which was up-regulated by combination with M-CSF. Our findings help to further understand the mechanisms regulating HIV-1 replication in MF, and the survival and M1/M2 ratio of MF.
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