BRF1 ameliorates LPS-induced inflammation through autophagy crosstalking with MAPK/ERK signaling

BRF1 通过自噬与 MAPK/ERK 信号转导相互作用改善 LPS 诱导的炎症

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作者:Weiwei Xie, Wei Zheng, Min Liu, Qizhong Qin, Yunpeng Zhao, Zhi Cheng, Fengjin Guo

Abstract

Inflammation is indispensable for host defense, whereas excessive inflammation often develop inflammatory diseases. Autophagy is thought to be engaged in many extracellular stress responses, such as starvation and innate immunity. Thus, autophagy plays an important role in maintaining homeostasis. The purpose of this study was to elucidate the function of BRF1 in the regulation of inflammation and autophagy response in macrophages. We found that BRF1 inhibited the LPS-induced inflammatory factors expression and the autophagy flux in macrophage. Furthermore, inhibition autophagy with 3-MA can attenuate the suppressive effect of BRF1 on LPS-mediated inflammation. In addition, MAPK/ERK signaling pathway was involved in the BRF1 inhibition inflammation and autophagy in macrophages. These findings indicate that BRF1 attenuates LPS-induced inflammatory factors secretion through autophagy, at least in part, through MAPK/ERK signaling pathway.

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