Dietary zinc and the control of Streptococcus pneumoniae infection
Dietary zinc and the control of Streptococcus pneumoniae infection
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DOI：
10.1371/journal.ppat.1007957
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发表时间：
2019-08-01
期刊：
影响因子：
6.7
通讯作者：
Mcdevitt, Christopher A.
中科院分区：
文献类型：
--
作者：
Eijkelkamp, Bart A.;Morey, Jacqueline R.;Mcdevitt, Christopher A.
人类缺锌增加对细菌感染的易感性。虽然锌补充疗法可以减少疾病的影响，但保护的分子基础仍不清楚。肺炎链球菌是细菌性肺炎的主要原因，在缺锌地区流行。我们报告，膳食锌水平决定的结果，S。肺炎病毒感染的小鼠模型。饮食锌限制影响小鼠组织锌水平与分布感染后改变，和S。肺炎菌毒力和感染性增强。虽然小鼠吞噬细胞的活化和浸润不受锌限制的影响，但其细菌控制的功效受到损害。S.肺炎链球菌对锌中毒高度敏感，在锌限制小鼠和分离的吞噬细胞中该过程受损。总的来说，这些数据显示了膳食锌缺乏如何增加对S。肺炎感染，同时揭示锌作为宿主抗微生物防御的组分的作用。
Human zinc deficiency increases susceptibility to bacterial infection. Although zinc supplementation therapies can reduce the impact of disease, the molecular basis for protection remains unclear. Streptococcus pneumoniae is a major cause of bacterial pneumonia, which is prevalent in regions of zinc deficiency. We report that dietary zinc levels dictate the outcome of S. pneumoniae infection in a murine model. Dietary zinc restriction impacts murine tissue zinc levels with distribution post- infection altered, and S. pneumoniae virulence and infection enhanced. Although the activation and infiltration of murine phagocytic cells was not affected by zinc restriction, their efficacy of bacterial control was compromised. S. pneumoniae was shown to be highly sensitive to zinc intoxication, with this process impaired in zinc restricted mice and isolated phagocytic cells. Collectively, these data show how dietary zinc deficiency increases sensitivity to S. pneumoniae infection while revealing a role for zinc as a component of host antimicrobial defences.