| Project/Area Number |
12670445
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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 |
内科学一般
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| Research Institution | Kinki University School of Medicine |
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Principal Investigator |
MATSUMARU Haruo Kinki University School of Medicine, Dept of Immunilcy, lecturer, 医学部, 講師 (10229536)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIE Osamu Kinki University School of Medicine, Dept of Bacterology, Professor, 医学部, 教授 (10166910)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2000: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | chemokine / hybridoma / hamster / Salmonella / monoclonal antibody / mucosal immunity / peroral immunization / peroral infection |
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| Research Abstract |
This research is to investigate the role of mouse CC chemokine LARC at intestine and lymphoid organ in mice infected with Salmonella. We planed to use non-immune mice and mice immunized perorally with avirulent strain of Salmonella typhimurium for the analysis of primary immune response and secondary immune response respectively after challenge with the virulent strain of Salmonella typhimurium.
We tried to establish anti-mouse LARC neutralizing antibody producing hybridoma for the analysis in vivo. We established several clones which bind to mouse LARC, but none of them was neutralizing antibody.
We established experimental conditions for peroral immunization and peroral challenge of Salmonella typhimurium. Based on that conditions, intestinal tract, liver and spleen were collected from infected or uninfected mice before the challenge or after the challenge at several time point. These tissues are processing for the analysis of an expression of LARC and distribution of cells.
Further we analyzed mechanisms of production of human LARC by the stimulation of IL-1 and TNF a with human cell lines derived from intestinal tract and kidney epidermis. In these cells activation of NF- KB is necessary for the production of LARC with the stimulation of IL-1 and TNFα. And our results suggest that keratinocytes produce LARC upon stimulation with IL-1 and TNFα, and attract CCRG-expressing immature dendritic cells and memory/effector T cells into the dermis of atopic dermatitis.
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