Roles of inflammation response in microglia cell through Toll-like receptors 2/interleukin-23/interleukin-17 pathway in cerebral ischemia/reperfusion injury

Abstract

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 interleukin-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.