1993 Fiscal Year Final Research Report Summary
In vitro model of blood-brain barrier in the autoimmune central nervous system disorders.
| Project/Area Number |
03670416
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Shinshu University |
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Principal Investigator |
KOH Shosei Shinshu University Hospital Department of Medicine (Neurology) Assistant Professor, 医学部・付属病院, 講師 (80143981)
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| Project Period (FY) |
1991 – 1993
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| Keywords | Blood-brain barrier / experimental autoimmune encephalomyelitis / multiple sclerosis / vascular endothelial cell / oligodendroglia |
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| Research Abstract |
Experimental autoimmune encephalomyelitis (EAE) is an autoimmune diseaase of central nervous system (CNS) myelin which can be induced in various species by a single injection of CNS tissue or isolated myelin basic protein (MBP), in combination with appropriate immunological adjuvants. EAE provides a model neuroautoimmune animal disease with clinical and immunohistopathologic similarities to human demyelinating disorders, e.g., multiple sclerosis (MS). Considerable evidence exists that activated T lymphocytes, reactive with myelin in general and MBP in particular, represent an important immune effector mechanism responsible for the inflammatory events underlying EAE and MS.Two closely related and as yet unresolved issues concerning EAE and MS are : 1) the anatomic site at which the host immune effector initially affects brain and spinal cord target tissue and 2) the specific events following this initial effector-target interaction that result in the development of neurologic disease. To resolve this issues we have established in vitro model of blood-brain barrier (BBB) by culturing brain vascular endothelial cells and oligodendroglia cells. We have measured BBB permeability by nsing this in vitro model and studied effects of inflammatory cytokines on BBB permeability. We have found that some of inflammatory cytokines are increasing factrt of BBB permeability. Some of cytokines induced procoagulant and/or fibrinolytic enzymes and injured oligodendroglia.
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