Research Centre for Infectious Diseases, Department of Molecular and Biomedical Science, School of Biological Sciences, The University of Adelaide, Adelaide, Australia.
Department of Molecular and Biomedical Science, School of Biological Sciences, The University of Adelaide, Adelaide, Australia.
PLoS Pathog. 2019 Aug 22;15(8):e1007957. doi: 10.1371/journal.ppat.1007957. eCollection 2019 Aug.
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.
人体缺锌会增加细菌感染的易感性。虽然补锌治疗可以减轻疾病的影响,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病因,在缺锌地区很常见。我们报告说,饮食中的锌水平决定了小鼠模型中肺炎链球菌感染的结果。饮食中锌的限制会影响小鼠组织中的锌水平,感染后分布发生改变,肺炎链球菌的毒力和感染增强。虽然锌限制不会影响小鼠吞噬细胞的激活和浸润,但它们控制细菌的效果受损。研究表明,肺炎链球菌对锌中毒非常敏感,而在缺锌的小鼠和分离的吞噬细胞中,这一过程受到了损害。总的来说,这些数据表明饮食中缺锌如何增加对肺炎链球菌感染的敏感性,同时揭示了锌作为宿主抗菌防御的一个组成部分的作用。