期刊
SCIENCE
卷 319, 期 5865, 页码 962-965出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1152449
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资金
- Engineering and Physical Sciences Research Council [GR/S98696/01, GR/S98689/01] Funding Source: researchfish
- NCI NIH HHS [P50 CA068485] Funding Source: Medline
- NHLBI NIH HHS [T32 HL069765] Funding Source: Medline
- NIAID NIH HHS [F32 AI071487] Funding Source: Medline
- NIGMS NIH HHS [R01 GM62112, T32 GM08320, 5R01 GM58008-09, T32 GM008320] Funding Source: Medline
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.
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