Lipopolysaccharide promotes NLRP3 inflammasome activation by inhibiting TFEB-mediated autophagy in NRK-52E cells

文献类型： 外文期刊

第一作者： Song, Dan

作者： Song, Dan;Tao, Wenjing;Liu, Feng;Wu, Xian;Bi, Haiyang;Wang, Dong;Li, Xiangchen;Song, Dan;Tao, Wenjing;Liu, Feng;Wu, Xian;Bi, Haiyang;Li, Xiangchen;Song, Dan;Tao, Wenjing;Liu, Feng;Wu, Xian;Bi, Haiyang;Wang, Dong;Li, Xiangchen;Song, Dan;Tao, Wenjing;Liu, Feng;Wu, Xian;Bi, Haiyang;Wang, Dong;Li, Xiangchen;Shu, Jianhong;Shu, Jianhong;Wang, Dong

作者机构：

关键词： Lipopolysaccharide; NLRP3; Inflammation; TFEB; Autophagy

期刊名称：MOLECULAR IMMUNOLOGY （ 影响因子：3.6； 五年影响因子：4.0 ）

ISSN： 0161-5890

年卷期： 2023 年 163 卷

页码：

收录情况： SCI

摘要： The NLRP3 inflammasome is involved in many inflammatory diseases. Its activity must be strictly controlled to alleviate the inflammatory process. Autophagy plays a protective role in the negative regulation of NLRP3 inflammasome activation. However, the regulatory mechanism of autophagy controlling NLRP3 inflammasome activation remains to be further investigated. Here, we showed that in NRK-52E cells, lipopolysaccharide (LPS) and ATP stimulation significantly decreased mitochondrial membrane potential, increased ROS production and mtDNA copy number in cytosol. Moreover, autophagic flux was blocked when challenged with LPS and ATP as evidenced by increased LC3 II and p62 expression, reduced TFEB and CTSD expression, and impaired lysosomal acid environment. Furthermore, TFEB deficiency increased cytosolic mtDNA and enhanced LPS and ATP induced NLRP3 inflammasome activation and proinflammatory cytokine expression. Taken together, these findings reveal that LPS and ATP stimulation promoted NLRP3 inflammasome activation through inhibiting TFEBmediated autophagy in NRK-52E cells, and TFEB could be a potential therapeutic target for the treatment of NLRP3 inflammasome-related kidney diseases.

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