• Zhizhen Zou, Xiling Deng, Jie Zhang, Jiangtao Dong, Fang Xu, Hui Zhang, Zhengyong Zhao, Xiaoling Liu, Su Liang, Jiangdong Wu, Le Zhang, Fang Wu, and Wanjiang Zhang.
• Department of Pathophysiology, Shihezi University School of Medicine/The Key Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi, Xinjiang Uyghur Autonomous Region, P.R. China.
• J. Investig. Med. 2024 Aug 1; 72 (6): 553566553-566.

AbstractLiver and lung tissue damage caused by sepsis is still one of the causes of death. B-lymphocyte-induced maturation protein-1 (Blimp-1) has a protective role in inflammation-related disease. However, whether Blimp-1 can regulate cell pyroptosis and affect disease progression in sepsis is still unclear. Animal and cell models were established by the cecal ligation and puncture method and lipopolysaccharides (LPS)-induced RAW 264.7 cells, respectively, and the role of Blimp-1 in regulation inflammatory response and pyroptosis was verified. The changes of inflammation and pyroptosis in liver and lung tissues of septic mice were determined by the addition of TAK-242 (TLR4 inhibitor). Cell pyroptosis and the level of inflammation was detected after Blimp-1 knockdown and TAK-242 treatment in the cell model. The expression of Blimp-1 was continuously increased in a septic mice model. After treatment with TAK-242, the expression of Blimp-1, pyroptosis and inflammatory levels were reduced in mice. In the LPS-induced cell model, cell injury by knockout Blimp-1 was increased, and cell activity was restored after TAK-242 intervention. Overexpression of Blimp-1 relieved LPS-induced cellular inflammatory damage and pyroptosis. Our study had shown that Blimp-1 could improve septic damage by regulating the level of cellular inflammation and pyroptosis in sepsis.

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