Dietary zinc and the control of Streptococcus pneumoniae infection

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dietary Supplements*
  • Disease Models, Animal*
  • Female
  • Lung Diseases / drug therapy
  • Lung Diseases / immunology*
  • Lung Diseases / microbiology
  • Mice
  • Pneumococcal Infections / drug therapy
  • Pneumococcal Infections / immunology*
  • Pneumococcal Infections / microbiology
  • Streptococcus pneumoniae / drug effects
  • Streptococcus pneumoniae / growth & development
  • Streptococcus pneumoniae / immunology*
  • Virulence / drug effects*
  • Zinc / administration & dosage*


  • Zinc

Grant support

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. This work was supported by the National Health and Medical Research Council (NHMRC; by Project Grant 1080784 to C.A.M., 1122582 to A.G.M., P.A.D. and C.A.M., and Program Grant 1071659 to J.C.P. This work was also supported by Australian Research Council (ARC; Discovery Project Grants DP170100036 and DP190102361 to P.A.D. and DP170102102 to J.C.P. and C.A.M. S.L.N. is a NHMRC Doherty Early Career Fellow (1142695), D.C. is funded by the Deutsche Forschungsgemeinschaft (German Research Foundation – 417283954) (, C.L.O. is a Garnett Passe and Rodney Williams Memorial Foundation ( Research Fellow and C.A.M. is an ARC Future Fellow (FT170100006).