2014 Fiscal Year Final Research Report
Formation of blood-brain barrier and activation of Interleukin-6 amplifier
Project/Area Number |
24390098
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Experimental pathology
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Research Institution | Hokkaido University (2013-2014) Osaka University (2012) |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2015-03-31
|
Keywords | 神経活性化 / 炎症回路 / 慢性炎症 / 神経反射シグナル |
Outline of Final Research Achievements |
Activation of NFkB and STAT induces massive production of chemokines in non-immune cells, which leads to local inflammation. We have been studying this inflammation amplifying mechanism, termed inflammation amplifier. In this study, we aimed to characterize mechanisms by which immune cells infiltrate into the central nervous system (CNS), and regulation of blood-brain barrier. In a murine model of multiple sclerosis, EAE, we found that high-performance MRI revealed that inflammation with edema occurred at fifth lumbar region where immune cells firstly enter the CNS. In addition, this edema was associated with ischemia/reperfusion injury that deteriorated the CNS inflammation. We also discovered that various stresses modulated the entry sites of immune cells into the CNS and altered the development of EAE in mice.
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Free Research Field |
免疫学
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