IL-17A induces autophagy and promotes microglial neuroinflammation through ATG5 and ATG7 in intracerebral hemorrhage

Microglial inflammation plays a vital role in intracerebral hemorrhage (ICH)-induced secondary brain injury. IL-17A has been identified to promote microglia activation, but the role in the pathology following ICH remains unclear. Autophagy is involved in modulation of cell metabolism, cell survival, and immune response. However, the role of IL-17A in autophagy following ICH has not been well defined. In this study, we assessed the role of IL-17A in microglial autophagic activity following ICH. The microglia were treated with IL-17A, and then autophagy and inflammation were detected. In addition, RNA interference in essential autophagy genes (ATG5 and ATG7) was also utilized to analyze microglial autophagy in vitro. Furthermore, ICH mice were made by injection of autologous blood model in vivo. And the IL-17A-neutralizing antibody was utilized to assess the neurological scores and brain edema. These data demonstrated that IL-17A promoted microglial autophagy and microglial inflammation. The suppression of autophagy using RNA interference in essential autophagy genes (ATG5 and ATG7) decreased microglial autophagy and inflammation. Moreover, IL-17A Ab significantly reduced brain water content and improved neurological function of ICH mice. Taken together, these data demonstrated that IL-17A promoted microglial autophagy and microglial inflammation, and IL-17A-mediated activation of autophagy might represent novel clues in ICH therapy.