| Project/Area Number |
06680751
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Nerve anatomy/Neuropathology
|
|---|
| Research Institution | Tokyo Metropolitan Institute for Neuroscience |
|---|
Principal Investigator |
MATSUMOTO Yoh Tokyo Metropolitan Institute for Neuroscience, Department of Neuropathology, Director, 神経病理研究部門, 副参事研究員 (90173921)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ISHIHARA Yoshihiro Tokyo Metropolitan Institute for Neuroscience, Department of Neuropathology, Dir, 神経病理研究部門, 副参事研究員 (50079711)
ABE Satoshi Niigata University, Brain Research Institute, Department of Neuropathology, Rese, 脳研究所神経病理, 助手 (90202663)
|
|---|
| Project Period (FY) |
1994 – 1995
|
| Project Status |
Completed (Fiscal Year 1995)
|
| Budget Amount *help |
¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
|
|---|
| Keywords | Autoimmune encephalomyelitis / Neural graft / Cytokines / Quantitative PCR / in situ RT-PCR / in situ RT-PCR |
|---|
| Research Abstract |
In the present study, we investigated the role of cytokines secreted in the lesion in the central nervous system (CNS) and cytokine network.Since the amount of cytokine protein and mRNA expressed in the CNS is very little, it was very difficult to examine them by ordinary methods such as Western and Northern blot analysis.Instead, using the experimental autoimmune encephalomyelitis (EAE) and neural tissue grafting model, we tried to establish the quantitative analysis of cytokine mRNA after amplification by the PCR techniques, i.e., competitive PCR.
In acute and monophasic rat EAE,both pro-inflammatory )IFN-gamma and TNF-alpha) and anti-inflammatory (IL-10) cytokines reached a maximal at the early stage of EAE suggesting the nature of its clinical course.On the other hand, in the graft rejection processes, mRNA for cytolytic protein such as perforin and granzyme B was expressed markedly.These disease-specific cytokine secretion profile strongly suggest that the nature of the lesion formed in the CNS regulates the mode of the lesion repair by modulating the cytokine network formed in the brain.
|
