B-lymphocyte-induced maturation protein-1 inhibits inflammation and pyroptosis to alleviate sepsis injury

Liver 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 unclea...

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Veröffentlicht in:Journal of investigative medicine 2024-08, Vol.72 (6), p.553-566
Hauptverfasser: Zou, Zhizhen, Deng, Xiling, Zhang, Jie, Dong, Jiangtao, Xu, Fang, Zhang, Hui, Zhao, Zhengyong, Liu, Xiaoling, Liang, Su, Wu, Jiangdong, Zhang, Le, Wu, Fang, Zhang, Wanjiang
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Sprache:eng
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Zusammenfassung:Liver 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.
ISSN:1081-5589
1708-8267
1708-8267
DOI:10.1177/10815589241249994