ROLES OF INFLAMMATION RESPONSE IN MICROGLIA CELL THROUGH TOLL-LIKE RECEPTORS 2/INTERLEUKIN-23/INTERLEUKIN-17 PATHWAY IN CEREBRAL ISCHEMIA/REPERFUSION INJURY

摘要

Microglial activation is one of the causative factors of neuroinflammation in cerebral ischemia. Activation via Toll-like receptors (TLRs) causes increased proinflammatory cytokine expression, such as interleukin-23 (IL-23) and inter-leukin-17 (IL-17), leading to inflammatory immune responses and neuronal damage. In this study, using a rat focal cerebral ischemia reperfusion (IR) model and an in vitro oxygen-glucose deprivation reperfusion (OGDR) system, we found that TLR2, IL-23 and IL-17 form an axis that leads to increased neuronal apoptosis. TLR2 activation results in IL-23 production which stimulates IL-17 production by microglia. This microglial axis may be a potential therapeutic target to control neuroinflammation in brain IR.