| Project/Area Number |
18590401
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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 |
Parasitology (including Sanitary zoology)
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| Research Institution | Nagasaki University |
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Principal Investigator |
HONMA Kiri Nagasaki University, Graduate school of Biomedical Sciences, Lecturer (70307940)
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| Co-Investigator(Kenkyū-buntansha) |
YUI Ktsuyuki Nagasaki University, Graduate school of Biomedical Sciences, Professor (90274638)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,020,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | IRF-4 / proinflammatory cvtokines / Leishmania major / macronhages / L.major |
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| Research Abstract |
(A)When L.major infected to IRF-4 deficient macrophages in vivo, footpad thickness increased at the early stage (2-5 weeks after infection)compared to wild type.
(B)The rate of the L.major infection was same between IRF-4 deficient macrophages and wild-type cells. However, the proportion of the infected macrophages remarkably decreased compared to wild type when L.major infected to IRF-4 deficient macrophages for 48 hrs in vitro, suggested that IRF-4 negatively regulated exclusion of L.major from the infected macrophages. TNF-α and NO from IRF-4 deficient, L.major-infected macrophages produced much higher than wild-type. Interestingly, IL-12 from IRF-4 deficient, and L.major infected macrophages produced much lower than wild-type. We expected that signaling to recognize L.major was different from TLR signaling because we have already reported that both IL-12 and TNF-α production through TLR remarkably enhanced in IRF-4 deficient macrophages. Alternation of cytokine production in IRF-4 KO macrophages to infect with L.major regulated at the transcriptional level. Various kind of denatured L.major antigens were made to identify major L.major molecule. Heat denatured or Proteinase K treated L.major antigen did not affect cytokine production pattern of TNF-α or IL-12 in IRF-4 KO macrophages. L.major molecule contained in insoluble fraction and was Proteinase K resistant molecule. It suggested that major antigen was not protein. And it was impossible to use ion exchange chromatography such as Bio-Cad.
(C)To separate L.major antigen, gel filtration method have been performed because it was able to separate each molecules by molecular weight.
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