Interleukin 17A exacerbates ER-stress-mediated inflammation of macrophages following ICH

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HighlightsIL-17A induced ER stress in macrophages and promoted inflammation in vitro.ERK 1/2 and p38 MAPK pathways contributed to IL-17A induced ER stress of macrophage.ER stress inhibition significantly attenuated brain water content and brain injury of ICH mice.IL-17A induced ER stress represented a novel clue in ICH.IL-17A contributes to the initiation of inflammation following intracerebral hemorrhage (ICH). Endoplasmic reticulum (ER) stress acts on protein folding and contributes to inflammatory diseases. The role of IL-17A in the regulation of ER stress following ICH has not been well characterized. In this study, macrophages were stimulated with IL-17A, and then, ER stress and downstream pro-inflammatory factors were measured in vitro. In addition, brain edema and brain injury in ICH mice were assessed in vivo. We demonstrated that IL-17A induced ER stress in macrophages and thus promoted inflammation in vitro. Conversely, IL-17A inhibition attenuated ER stress and neuroinflammation. Furthermore, ERK 1/2 and p38 MAPK pathways mediated IL-17A-induced ER stress in macrophages. We also showed that IL-17A inhibition significantly attenuated ER stress and brain injury in ICH mice.In conclusion, our results demonstrate that IL 17A increases ER stress in macrophages and represents a novel mechanism in ICH.

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