| Literature DB >> 28943329 |
Lillian J Juttukonda1, Evelien T M Berends2, Joseph P Zackular1, Jessica L Moore3, Matthew T Stier1, Yaofang Zhang4, Jonathan E Schmitz1, William N Beavers1, Christiaan D Wijers1, Benjamin A Gilston5, Thomas E Kehl-Fie6, James Atkinson1, Mary K Washington1, R Stokes Peebles7, Walter J Chazin8, Victor J Torres2, Richard M Caprioli9, Eric P Skaar10.
Abstract
Diet, and specifically dietary metals, can modify the risk of infection. However, the mechanisms by which manganese (Mn), a common dietary supplement, alters infection remain unexplored. We report that dietary Mn levels dictate the outcome of systemic infections caused by Staphylococcus aureus, a leading cause of bacterial endocarditis. Mice fed a high Mn diet display alterations in Mn levels and localization within infected tissues, and S. aureus virulence and infection of the heart are enhanced. Although the canonical mammalian Mn-sequestering protein calprotectin surrounds staphylococcal heart abscesses, calprotectin is not released into the abscess nidus and does not limit Mn in this organ. Consequently, excess Mn is bioavailable to S. aureus in the heart. Bioavailable Mn is utilized by S. aureus to detoxify reactive oxygen species and protect against neutrophil killing, enhancing fitness within the heart. Therefore, a single dietary modification overwhelms vital host antimicrobial strategies, leading to fatal staphylococcal infection.Entities:
Keywords: Staphylococcus aureus; bacterial pathogenesis; calprotectin; diet; endocarditis; manganese; neutrophils; nutritional immunity; oxidative stress
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Year: 2017 PMID: 28943329 PMCID: PMC5638708 DOI: 10.1016/j.chom.2017.08.009
Source DB: PubMed Journal: Cell Host Microbe ISSN: 1931-3128 Impact factor: 21.023