Suppr超能文献

鼠伤寒沙门氏菌中的反应性多硫化物通过抑制亲电信号抑制自噬介导的巨噬细胞固有免疫。

Reactive Persulfides from Salmonella Typhimurium Downregulate Autophagy-Mediated Innate Immunity in Macrophages by Inhibiting Electrophilic Signaling.

机构信息

Gladstone Institute of Virology and Immunology, University of California, San Francisco, CA 94158, USA.

Department of Environmental Medicine and Molecular Toxicology, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.

出版信息

Cell Chem Biol. 2018 Nov 15;25(11):1403-1413.e4. doi: 10.1016/j.chembiol.2018.08.007. Epub 2018 Sep 6.

Abstract

Reactive persulfides such as cysteine persulfide and glutathione persulfide are produced by bacteria including Salmonella during sulfur metabolism. The biological significance of bacterial reactive persulfides in host-pathogen interactions still warrants investigation. We found that reactive persulfides produced by Salmonella Typhimurium LT2 regulate macrophage autophagy via metabolizing 8-nitroguanosine 3',5'-cyclic monophosphate (8-nitro-cGMP), an electrophilic product of reactive oxygen species and nitric oxide signaling. 8-Nitro-cGMP signaling was required for efficient autophagy-mediated clearance of Salmonella from infected macrophages. In the infected cells, 8-nitro-cGMP caused cGMP adduct formation (S-guanylation) of bacterial surface proteins, which triggered recruitment of autophagy-related proteins p62 and LC3-II to the intracellular bacteria. We also found that Salmonella-produced reactive persulfides downregulated this autophagy by decreasing cellular 8-nitro-cGMP content, thereby inhibiting electrophilic signaling. These data reveal a pathogenic role of bacteria-derived reactive persulfides via suppression of anti-bacterial autophagy.

摘要

反应性过硫化物,如半胱氨酸过硫化物和谷胱甘肽过硫化物,是由包括沙门氏菌在内的细菌在硫代谢过程中产生的。细菌反应性过硫化物在宿主-病原体相互作用中的生物学意义仍有待研究。我们发现,鼠伤寒沙门氏菌 LT2 产生的反应性过硫化物通过代谢活性氧和一氧化氮信号的亲电子产物 8-硝基鸟苷 3',5'-环单磷酸(8-nitro-cGMP)来调节巨噬细胞自噬。8-nitro-cGMP 信号对于从感染的巨噬细胞中有效清除沙门氏菌所必需的自噬介导清除至关重要。在感染的细胞中,8-nitro-cGMP 导致细菌表面蛋白的 cGMP 加合物形成(S-鸟嘌呤化),这触发了自噬相关蛋白 p62 和 LC3-II 向细胞内细菌的募集。我们还发现,沙门氏菌产生的反应性过硫化物通过降低细胞内 8-nitro-cGMP 含量来抑制这种自噬,从而抑制亲电信号。这些数据揭示了细菌衍生的反应性过硫化物通过抑制抗细菌自噬来发挥致病作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验