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[大肠杆菌EscI蛋白C末端肽诱导巨噬细胞中的炎性小体反应]

[Inflammasome responses in macrophages induced by C-terminal peptides of Escherichia coli EscI protein].

作者信息

Hu Maozhi, Li Wenhua, Yan Qiuxiang, Geng Shizhong, Pan Zhiming, Cui Guiyoui, Jiao Xin'an

出版信息

Wei Sheng Wu Xue Bao. 2015 Oct 4;55(10):1350-5.

Abstract

OBJECTIVE

To analyze NLRC4 inflammasome responses in macrophages induced by C-terminal of Escherichia coli EscI protein.

METHODS

NLRC4 inflammasome responses in mouse peritoneal macrophages were analyzed after delivery of the peptides containing C-terminal amino acid sequences of E. coli EscI protein in vitro.

RESULTS

The peptides containing C-terminal 15 amino acids of EscI protein could significantly activate NLRC4 inflammasome responses in macrophages pre-stimulated with lipopolysaccharide. Intracellular caspase-1 was activated and pyroptotic dead cells were found after peptides delivery. The contents of cytokines, IL-1β and IL-18, in supernatants were elevated significantly compared with that of the control (P < 0.05). Besides, through comparison of IL-1β contents under different stimulation conditions, 4 h incubation after peptides delivery (peptides: lipofectamine 2000 = 70 μg/μL) could obviously promote the secretion of IL-1β.

CONCLUSION

Peptides containing C-terminal 15 amino acids of E. coli EscI protein can significantly induce NLRC4 inflammasome activation in macrophages.

摘要

目的

分析大肠杆菌EscI蛋白C端诱导巨噬细胞中NLRC4炎性小体的反应。

方法

在体外递送含有大肠杆菌EscI蛋白C端氨基酸序列的肽后,分析小鼠腹腔巨噬细胞中NLRC4炎性小体的反应。

结果

含有EscI蛋白C端15个氨基酸的肽可显著激活经脂多糖预刺激的巨噬细胞中NLRC4炎性小体的反应。递送肽后,细胞内半胱天冬酶-1被激活,并发现细胞发生焦亡。与对照组相比,上清液中细胞因子IL-1β和IL-18的含量显著升高(P < 0.05)。此外,通过比较不同刺激条件下IL-1β的含量,递送肽后孵育4小时(肽:脂质体2000 = 70 μg/μL)可明显促进IL-1β的分泌。

结论

含有大肠杆菌EscI蛋白C端15个氨基酸的肽可显著诱导巨噬细胞中NLRC4炎性小体的激活。

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