Relationship between the neuroprotection by brain hypothermia and the temporal IL-23 - IL-17 production by immune cells

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462403
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Anesthesiology
• Research Institution: Yamaguchi University
• Principal Investigator: MATSUI Tomohiro 山口大学, 医学(系)研究科(研究院), 講師 (50314828)
• Co-Investigator(Renkei-kenkyūsha): KIDA Hiroyuki 山口大学, 大学院医学系研究科, 助教 (70432739)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 脳低温療法 / T細胞 / インターロイキン17 / グランザイムB / 高温培養 / ニューロン死 / 脳血管内皮細胞

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.

Free Research Field

神経免疫学