| Project/Area Number |
21592097
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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 |
Obstetrics and gynecology
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| Research Institution | Tottori University |
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Principal Investigator |
IWABE Tomio 鳥取大学, 医学部, 准教授 (10284001)
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| Co-Investigator(Kenkyū-buntansha) |
DEURA Imari 鳥取大学, 医学部附属病院, 助教 (50464293)
月原 悟 鳥取大学, 医学部附属病院, 助教 (80448191)
堀江 さや子 鳥取大学, 医学部附属病院, 助教 (60464294)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 子宮内膜症 / 子宮内膜 / 炎症性サイトカイン / 3次元培養系 / 3次元培養 / TNFα / インターロイキン6 / インターロイキン8 / TNFalpha / 月経血 / 組織培養 |
|---|
| Research Abstract |
1. We examined the effect of menstrual blood on the ability of cytokine production in these immune cells. We examined the CD14+monocyte and DC were cultured the containing 2% or 10% menstrual blood in the culture medium for 24 hours, and measured the concentration of interleukin-6 and interleukin-8 in the supernatants with ELISA. We demonstrated that the menstrual blood induced the cytokine levels in the immune cells. These results suggest that retrograde menstruation may be contributed to the pathogenesis of endometriosis.
2 We examined the three-dimensional culture system. Endometrial and endometriotic stromal cells were obtained from normal endometrium and from chocolate cyst linings. We used Celltight X TM(SUMILON). We evaluate the effect of TNFa on those calls compared with monolayer culture systems. IL-6 and IL-8 protein production was examined by ELISA. Endometriotic stromal cells product the inflammatory cytokines without TNFa. The addition of TNFa promoted the production of inflammatory cytokines, compared with monolayer culture systems. These results suggested that the inflammatory cytokines work as the autocrine and paracrine factor for the proliferation of endometriotic cells
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