期刊
JOURNAL OF BACTERIOLOGY
卷 186, 期 17, 页码 5629-5639出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.186.17.5629-5639.2004
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资金
- NIGMS NIH HHS [GM55594, R01 GM019416, GM19416, F32 GM019416, R37 GM019416, R01 GM055594] Funding Source: Medline
Bacterial growth as a biofilm on solid surfaces is strongly associated with the development of human infections. Biofilms on native heart valves (infective endocarditis) is a life-threatening disease as a consequence of bacterial resistance to antimicrobials in such a state. Enterococci have emerged as a cause of endocarditis and nosocomial infections despite being normal commensals of the gastrointestinal and female genital tracts. We examined the role of two-component signal transduction systems in biofilm formation by the Enterococcus faecalis V583 clinical isolate and identified the fsr regulatory locus as the sole two-component system affecting this unique mode of bacterial growth. Insertion mutations in the fsr operon affected biofilm formation on two distinct abiotic surfaces. Inactivation of the fsr-controlled gene gelE encoding the zinc-metalloprotease gelatinase was found to prevent biofilm formation, suggesting that this enzyme may present a unique target for therapeutic intervention in enterococcal endocarditis.
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