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.