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1. Dietary Manganese Promotes Staphylococcal Infection of the Heart.

Author

Juttukonda LJ, Berends ETM, Zackular JP, Moore JL, Stier MT, Zhang Y, Schmitz JE, Beavers WN, Wijers CD, Gilston BA, Kehl-Fie TE, Atkinson J, Washington MK, Peebles RS, Chazin WJ, Torres VJ, Caprioli RM, and Skaar EP

Subjects
Abscess, Animals, Diet, Disease Models, Animal, Heart physiopathology, Humans, Leukocyte L1 Antigen Complex metabolism, Liver microbiology, Liver physiopathology, Manganese analysis, Mice, Mice, Congenic, Mice, Inbred C57BL, Neutrophils metabolism, Reactive Oxygen Species metabolism, Staphylococcus aureus pathogenicity, Endocarditis, Bacterial microbiology, Heart microbiology, Manganese metabolism, Staphylococcal Infections microbiology, Staphylococcus aureus metabolism
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., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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2. The Response of Acinetobacter baumannii to Zinc Starvation.

Author

Nairn BL, Lonergan ZR, Wang J, Braymer JJ, Zhang Y, Calcutt MW, Lisher JP, Gilston BA, Chazin WJ, de Crécy-Lagard V, Giedroc DP, and Skaar EP

Subjects
Acinetobacter Infections microbiology, Acinetobacter baumannii genetics, Acinetobacter baumannii growth & development, Animals, Bacterial Proteins genetics, Bacterial Proteins metabolism, Chlorides metabolism, GTP Phosphohydrolases metabolism, Gene Expression Regulation, Bacterial, Genes, Bacterial, Histidine metabolism, Histidine Ammonia-Lyase metabolism, Metallochaperones genetics, Metallochaperones metabolism, Mice, Mice, Inbred C57BL, Mutation, Zinc metabolism, Zinc Compounds metabolism, Acinetobacter baumannii metabolism, Zinc deficiency
Abstract

Zinc (Zn) is an essential metal that vertebrates sequester from pathogens to protect against infection. Investigating the opportunistic pathogen Acinetobacter baumannii's response to Zn starvation, we identified a putative Zn metallochaperone, ZigA, which binds Zn and is required for bacterial growth under Zn-limiting conditions and for disseminated infection in mice. ZigA is encoded adjacent to the histidine (His) utilization (Hut) system. The His ammonia-lyase HutH binds Zn very tightly only in the presence of high His and makes Zn bioavailable through His catabolism. The released Zn enables A. baumannii to combat host-imposed Zn starvation. These results demonstrate that A. baumannii employs several mechanisms to ensure bioavailability of Zn during infection, with ZigA functioning predominately during Zn starvation, but HutH operating in both Zn-deplete and -replete conditions to mobilize a labile His-Zn pool., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Published
2016
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