| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
T cells infiltrate into the infarcted brain within days after cerebral ischemia and play essential roles in exacerbating the delayed phase of the brain injury by producing pro-inflammatory factors. However, the involvement of these factors in brain damage is also demonstrated systemically. Such periphery-brain abnormalities are interesting because they may constitute a pathway to the central nervous system, which may be a target of therapeutic hypothermia. We examined the effects of hypothermia and hyperthermia on peripheral T cell-derived release of IL-17 and granzyme B (GrB). As a result, compared with normothermia, IL-17 and GrB release was reduced by hypothermia but augmented by hyperthermia. Moreover, IL-17 and GrB caused the death of neuronal cells in a concentration-dependent manner. These results suggest that the attenuation of T cell-derived release of IL-17 and GrB by therapeutic hypothermia leads to the inhibition of neuronal cell death in the delayed phase of brain injury.
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