病原体在宿主组织中感受和克服镁限制的机制。
How Pathogens Feel and Overcome Magnesium Limitation When in Host Tissues.
机构信息
Laboratory of Pathogen Host Interactions, Université Montpellier, case 107, Place Eugène Bataillon, 34095, Montpellier cedex 5, France; CNRS, UMR5235, 34095, Montpellier Cedex 05, France.
Department of Microbial Pathogenesis, Yale School of Medicine, 295 Congress Avenue, New Haven, CT 06536, USA; Yale Microbial Sciences Institute, P.O. Box 27389, West Haven, CT 06516, USA.
出版信息
Trends Microbiol. 2021 Feb;29(2):98-106. doi: 10.1016/j.tim.2020.07.003. Epub 2020 Aug 14.
Abstract
Host organisms utilize nutritional immunity to limit the availability of nutrients essential to an invading pathogen. Nutrients may include amino acids, nucleotide bases, and transition metals, the essentiality of which varies among pathogens. The mammalian macrophage protein Slc11a1 (previously Nramp1) mediates resistance to several intracellular pathogens. Slc11a1 is proposed to restrict growth of Salmonella enterica serovar Typhimurium in host tissues by causing magnesium deprivation. This is intriguing because magnesium is the most abundant divalent cation in all living cells. A pathogen's response to factors such as Slc11a1 that promote nutritional immunity may therefore reflect what the pathogen 'feels' in its cytoplasm, rather than the nutrient concentration in host cell compartments.
摘要
宿主生物利用营养免疫来限制入侵病原体所需的营养物质的可用性。这些营养物质可能包括氨基酸、核苷酸碱基和过渡金属，其必要性因病原体而异。哺乳动物巨噬细胞蛋白 Slc11a1（以前称为 Nramp1）介导对几种细胞内病原体的抗性。Slc11a1 通过引起镁缺乏来限制肠炎沙门氏菌血清型 Typhimurium 在宿主组织中的生长。这很有趣，因为镁是所有活细胞中含量最丰富的二价阳离子。因此，病原体对促进营养免疫的 Slc11a1 等因素的反应可能反映了病原体在细胞质中“感受到”的情况，而不是宿主细胞区室中的营养浓度。
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