肠道上皮细胞中的 LNCGM1082 可促进受感染上皮细胞的排出和 IL-18 的释放。

Q3 Medicine
Ya Wang, Yunhuan Gao, Xiaomin Su, Yang Hao, Yuan Zhang, Rongcun Yang
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引用次数: 0

摘要

炎症小体 NLRC4(NLR 家族 CARD 含域 4)可以保护肠道等粘膜屏障免受细菌病原体的入侵。然而,NLRC4如何在肠上皮细胞中被激活尚不完全清楚。在这项研究中,我们证实了LNCGM1082可通过将NLRC4与蛋白激酶C(PKC)δ结合来介导NLRC4的活化。LNCGM1082基因敲除(KO)小鼠对鼠伤寒沙门氏菌感染的抵抗力下降,受感染肠道上皮细胞的排出和IL-18的释放也受到影响。与 NLRC4 KO 和 PKCδ 敲除的肠道器官组织类似,LNCGM1082 KO 的肠道器官组织中肠道上皮细胞的排出和 IL-18 的释放也受到影响。此外,LNCGM1082 KO、NLRC4 KO和PKCδ敲除的肠道器官组织在接触鼠伤寒杆菌后,caspase-1和caspase-8的活化也有所降低。我们的研究结果表明,ICEs中的LNCGM1082通过与NLRC4和PKCδ结合,在介导NLRC4的活化方面起着关键作用,并在暴露于伤寒杆菌等细菌时促进受感染上皮细胞的排出和IL-18的释放。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LNCGM1082 in Gut Epithelial Cells Promotes Expulsion of Infected Epithelial Cells and Release of IL-18.

Inflammasome NLRC4 (NLR family CARD domain containing 4) can protect mucosal barriers such as intestine from invading bacterial pathogens. However, it was incompletely clear how NLRC4 was activated in intestinal epithelial cells. In this study, we demonstrated that LNCGM1082 could mediate the activation of NLRC4 via binding NLRC4 with protein kinase C (PKC)δ. LNCGM1082 knockout (KO) mice had reduced resistance against Salmonella Typhimurium infection, as well as impaired expulsion of infected gut epithelial cells and release of IL-18 upon exposure to S. Typhimurium. Similar to NLRC4 KO and PKCδ knockdown gut organoids, there also was impaired expulsion of gut epithelial cells and release of IL-18 in LNCGM1082 KO gut organoids. Furthermore, there also was reduced activation of caspase-1 and caspase-8 in these LNCGM1082 KO, NLRC4 KO, and PKCδ knockdown gut organoids upon exposure to S. Typhimurium. Our results show that LNCGM1082 in the ICEs plays a critical role in mediating activation of NLRC4 through binding NLRC4 and PKCδ and promoting expulsion of infected epithelial cells and release of IL-18 upon exposure to bacteria such as S. Typhimurium.

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来源期刊
CiteScore
3.70
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