| Project/Area Number |
16590352
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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 |
Bacteriology (including Mycology)
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| Research Institution | Hirosaki University |
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Principal Investigator |
NAKANE Akio Hirosaki University, School of Medicine, Professor, 医学部, 教授 (30164239)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Listeria monocytogenes / Infection / Leptin / Insulin / MCP-1 / KC / Urocortin / IL-10 / CRF / STAT3 / 肥満 / 糖尿病 |
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| Research Abstract |
Leptin is an adipocyte-derived hormone that regulates a number of physiological functions, including energy homeostasis and immune function. We investigated a role of leptin in Listeria monocytogenes infection using leptin receptor-deficient db/db mice and leptin-deficient ob/ob mice. These mutant mice were highly susceptible to L.monocytogenes and the elimination of bacteria from the livers was inhibited. After infection, the induction of MCP-1 and KC mRNA in the livers of db/db mice and the MCP-1 mRNA expression in those of ob/ob mice was decreased. Leptin replacement in ob/ob mice resulted in improvement of antilisterial resistance and the MCP-1 mRNA expression. The elimination of L.monocytogenes was significantly enhanced and the expression of MCP-1 and KC mRNA were completely reversed in db/db mice by insulin treatment. These results suggest leptin is required for host resistance to L.monocytogenes infection and that hyperglycemia caused by leptin deficiency is involved in the ine
… More
fficient elimination of bacteria from the livers. Moreover, defect of MCP-1 expression in liver may be involved in the attenuated host resistance in these mutant mice.
We investigated the effect of CRF family peptides on host resistance to Listeria monocytogenes infection in mice. When mice were administered with CRF, urocortin (Ucn) or Ucn2 before L.monocytogenes infection, the numbers of bacteria in the organs of Ucn2-treated mice were dramatically increased and most of these mice succumbed. IL-10 production was significantly increased and IFN-γ and TNF-α production was decreased in the spleens of Ucn2-treated mice. The effect of Ucn2 was canceled by treatment with anti-IL-10 monoclonal antibody and in IL-10 deficient mice. The expression and activation of STAT3 were up-regulated and the expression and activation of STAT1 were down-regulated in the spleens from Ucn2-treated mice. These results suggested that Urn2 suppresses host resistance to L.monocytogenes infection via up-regulation of IL-10 production Less
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