期刊
JOURNAL OF INFECTIOUS DISEASES
卷 210, 期 3, 页码 473-482出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiu091
关键词
Staphylococcus aureus; nuclease; clindamycin; immunoglobulin; molecular beacon; NET
资金
- Swiss National Science Foundation [310030_146295/1, PZ00P3_136639]
- Zentrum fur Klinische Forschung
- Stiftung fur Medizinische Forschung, University of Zurich
- Swiss National Science Foundation (SNF) [PZ00P3_136639] Funding Source: Swiss National Science Foundation (SNF)
The Gram-positive human pathogen Staphylococcus aureus causes a variety of human diseases such as skin infections, pneumonia, and endocarditis. The micrococcal nuclease Nuc1 is one of the major S. aureus virulence factors and allows the bacterium to avoid neutrophil extracellular trap (NET)-mediated killing. We found that addition of the protein synthesis inhibitor clindamycin to S. aureus LAC cultures decreased nuc1 transcription and subsequently blunted nuclease activity in a molecular beacon-based fluorescence assay. We also observed reduced NET degradation through Nuc1 inhibition translating into increased NET-mediated clearance. Similarly, pooled human immunoglobulin specifically inhibited nuclease activity in a concentration-dependent manner. Inhibition of nuclease activity by clindamycin and immunoglobulin enhanced S. aureus clearance and should be considered in the treatment of S. aureus infections.
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