Nutritional immunity beyond iron: a role for manganese and zinc.

Nutritional immunity beyond iron: a role for manganese and zinc.
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DOI:
10.1016/j.cbpa.2009.11.008
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发表时间:
2010-04
影响因子:
7.8
通讯作者:
Skaar, Eric P.
Skaar, Eric P.
中科院分区:
生物学2区
文献类型:
--
作者:
Kehl-Fie, Thomas E.;Skaar, Eric P.

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脊椎动物从入侵的病原体中隔离铁,相反,病原体表达多种因子从宿主中窃取铁。最近的研究表明,除了铁之外,脊椎动物还在细胞内和细胞外螯合锌和锰,以防止感染。在细胞内,脊椎动物分别利用ZIP/ZnT家族转运蛋白操纵锌水平,以及Nramp 1操纵锰水平。在细胞外,S100蛋白钙卫蛋白可螯合锰和潜在的锌,以抑制微生物生长。为了规避这些防御,细菌具有高亲和力的转运蛋白来输入特定的营养金属。限制锌和锰的可用性作为防御感染的机制,扩大了营养免疫的范围,并进一步建立了金属螯合作为对抗微生物入侵者的关键防御。
Vertebrates sequester iron from invading pathogens, and conversely, pathogens express a variety of factors to steal iron from the host. Recent work has demonstrated that in addition to iron, vertebrates sequester zinc and manganese both intracellularly and extracellularly to protect against infection. Intracellularly, vertebrates utilize the ZIP/ZnT families of transporters to manipulate zinc levels, as well as Nramp1 to manipulate manganese levels, respectively. Extracellularly, the S100 protein calprotectin sequesters manganese and potentially zinc to inhibit microbial growth. To circumvent these defenses, bacteria possess high affinity transporters to import specific nutrient metals. Limiting the availability of zinc and manganese as a mechanism to defend against infection expands the spectrum of nutritional immunity and further establishes metal sequestration as a key defense against microbial invaders.
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