2019年11月22日，瑞士巴塞尔大学Dirk Bumann团队在《科学》杂志发表论文，报道了宿主抗性因子SLC11A1通过镁离子剥夺来抑制沙门氏菌的生长。

研究人员比较了具有不同SLC11A1等位基因同类系小鼠的沙门氏菌感染。SLC11A1减少了沙门氏菌的复制并触发了对二价金属阳离子摄取系统的上调，但没有其他应激反应。 SLC11A1一定程度上降低了铁的利用率，并严重限制了沙门氏菌获取镁的途径。在SLC11A1存在下沙门氏菌细胞的生长高度异质，并且与关键的镁转运蛋白mgtB的表达呈负相关。

当通过减少沙门氏菌对镁的吸收来限制其摄入时，研究人员在缺乏SLC11A1的小鼠中观察到了类似的单细胞模式。因此，这些发现表明SLC11A1通过剥夺主族金属镁作为抵抗对沙门氏菌的主要机制。

据悉，多效性宿主抗性因子SLC11A1（NRAMP1）通过未知机制防御哺乳动物中多种细胞内病原体。

附：英文原文

Title: Host resistance factor SLC11A1 restricts Salmonella growth through magnesium deprivation

Author: Olivier Cunrath, Dirk Bumann

Issue&Volume: 2019/11/22

Abstract: The pleiotropic host resistance factor SLC11A1 (NRAMP1) defends against diverse intracellular pathogens in mammals by yet-unknown mechanisms. We compared Salmonella infection of coisogenic mice with different SLC11A1 alleles. SLC11A1 reduced Salmonella replication and triggered up-regulation of uptake systems for divalent metal cations but no other stress responses. SLC11A1 modestly diminished iron availability and acutely restricted Salmonella access to magnesium. Growth of Salmonella cells in the presence of SLC11A1 was highly heterogeneous and inversely correlated with expression of the crucial magnesium transporter gene mgtB. We observed superimposable single-cell patterns in mice lacking SLC11A1 when we restricted Salmonella access to magnesium by impairing its uptake. Together, these findings identify deprivation of the main group metal magnesium as the main resistance mechanism of SLC11A1 against Salmonella.

DOI: 10.1126/science.aax7898

Source: https://science.sciencemag.org/content/366/6468/995