| Project/Area Number |
13670261
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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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| Co-Investigator(Kenkyū-buntansha) |
MIURA Tomisato Hirosaki University, School of Medicine, Lecturer, 医学部, 講師 (20261456)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2001: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | Listeria monocytogenes / Sympathetic nerve system / Epinephrine receptor / MIF / IFN-gamma / TNF-alpha / IL-10 / Cortisol / 下垂体 / 神経系 / 細菌感染 |
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| Research Abstract |
The host defense mechanism against bacterial infections through catecholamine receptors was investigated. Furthermore, the role of macrophage migration inhibitory factor (MIF), which is known to mediate the crosstalk between immune system and nerve system, in bacterial infections was investigated.
1. The regulatory mechanism by catecholamines in host defense against bacterial infections. The in vivo effects of antagonists and agonists to epinephrine receptors on host defense against Listeria monocytgenes infection and cytokine responses were investigated. When epinephrine receptor α antagonists were injected into mice, antilisterial resistance and productions of IFN-γ and TNF-α were suppressed. In contrast, epimephrine receptor β antagonists revealed no significant effect on antilisterial resistance and the cytokine production. These results suggest that antilisterial resistance and productions of IFN-γ and TNF-α may be regulated by epinephrine receptor α.
2. The role of MIF in bacterial
… More
infections (1) Endogenous MIF levels in the infected organs were up-regulated by a lethal infection with L. monocytogenes. The administration of anti-MIF antibody into mice showed no significant effect on the fate of a sublethal infection with L. monocytogenes, whereas the antibody rescued the mice from a lethal infection with L. monocytogenes. (2) Endogenous IFN-γ and TNF-α production in the infected organs was up-regulated in the early phase but down-regulated in the late phase of lethal infection in anti-MIF antibody-treated mice. (3) Endogenous IL-10 production in the livers was up-regulated in anti-MIF antibody-treated mice. Abnormality of liver function was partially restored by the administration of anti-IL-10 antibody in anti-MIF antibody-treated mice. (4) The level of plasma cortisol was significantly low in anti-MIF antibody-treated mice, compared with that of the normal rabbit globulin-treated mice.
These results suggest that MIF is involved in the pathogensis of a lethal infection with L. monocytogenes through the regulation of IL-10 production. Less
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