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|Title:||Dietary zinc and the control of Streptococcus pneumoniae infection|
Gonzalez de Vega, R.
|Citation:||PLoS pathogens, 2019; 15(8):1-26|
|Bart A. Eijkelkamp, Jacqueline R. Morey, Stephanie L. Neville, Aimee Tan, Victoria G. Pederick, Nerida Cole, Prashina P. Singh, Cheryl-Lynn Y. Ong, Raquel Gonzalez de Vega, David Clases, Bliss A. Cunningham, Catherine E. Hughes, Iain Comerford, Erin B. Brazel, Jonathan J. Whittall, Charles D. Plumptre, Shaun R. McColl, James C. Paton, Alastair G. McEwan, Philip A. Doble, Christopher A. McDevitt|
|Abstract:||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.|
|Rights:||© 2019 Eijkelkamp et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
|Appears in Collections:||Microbiology and Immunology publications|
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