Metal chelation and inhibition of bacterial growth in tissue abscesses.

Corbin BD, Seeley EH, Raab A, Feldmann J, Miller MR, Torres VJ, Anderson KL, Dattilo BM, Dunman PM, Gerads R, Caprioli RM, Nacken W, Chazin WJ, Skaar EP
Science. 2008 319 (5865): 962-5

PMID: 18276893 · DOI:10.1126/science.1152449

Bacterial infection often results in the formation of tissue abscesses, which represent the primary site of interaction between invading bacteria and the innate immune system. We identify the host protein calprotectin as a neutrophil-dependent factor expressed inside Staphylococcus aureus abscesses. Neutrophil-derived calprotectin inhibited S. aureus growth through chelation of nutrient Mn2+ and Zn2+: an activity that results in reprogramming of the bacterial transcriptome. The abscesses of mice lacking calprotectin were enriched in metal, and staphylococcal proliferation was enhanced in these metal-rich abscesses. These results demonstrate that calprotectin is a critical factor in the innate immune response to infection and define metal chelation as a strategy for inhibiting microbial growth inside abscessed tissue.

MeSH Terms (16)

Abscess Animals Calcium Chelating Agents Dimerization Gene Expression Profiling Kidney Diseases Leukocyte L1 Antigen Complex Liver Abscess Manganese Mass Spectrometry Mice Neutrophils Staphylococcal Infections Staphylococcus aureus Zinc

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