IL-17A promotes microglial activation and neuroinflammation in mouse models of intracerebral haemorrhage

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Microglial activation is an important contributor to neuroinflammation in intracerebral haemorrhage (ICH). IL-17A has been demonstrated to be involved in neuroinflammatory diseases such as multiple sclerosis. However, the exact mechanism of IL-17A mediated microglial activation in ICH has not been well identified. The purpose of this experiment is to investigate the role of IL-17A in ICH induced microglial activation and neuroinflammation. ICH mice were made by injection of autologous blood model. IL-17A expression and inflammatory factors in perihematomal region, and neurological function of mice were examined after ICH. In addition, IL-17A-neutralizing antibody was utilized to potentially prevent microglial activation and neuroinflammation in ICH mice. The expression of IL-17A, inflammatory factors and microglial activation in perihematomal region were significantly increased, and neurological function of mice was impaired after ICH. In addition, IL-17A Ab prevented ICH-induced cytokine expression, including TNF-α, IL-1β and IL-6, and downstream signaling molecules, including MyD88, TRIF, IκBα, and NF-κBp65 expression, and attenuated microglial activation. IL-17A Ab significantly reduced brain water content and improved neurological function of ICH mice. In conclusion, our results demonstrated that IL-17A was involved in ICH-induced microglial activation and neuroinflammation. IL-17A Ab might also provide a promising therapeutic strategy in ICH.

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