Abstract
The mechanisms of antibiotic-induced cell death are poorly understood despite the critical role of the bactericidal activities of antibiotics for successful treatment of severe infections. These mechanisms include irreversible damaging of macromolecules by reactive oxygen species and bacteriolysis mediated by peptidoglycan hydrolases (autolysins). We have assessed the contribution of the second mechanism by using an autolysin-deficient mutant of Enterococcus faecalis and shown that it contributes to amoxicillin-induced cell lysis only at a high bacterial density.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amoxicillin / pharmacology*
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Animals
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Anti-Bacterial Agents / pharmacology*
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Bacteriolysis / drug effects*
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Colony Count, Microbial
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Endocarditis, Bacterial / drug therapy
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Endocarditis, Bacterial / microbiology
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Enterococcus faecalis / drug effects*
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Enterococcus faecalis / genetics
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Enterococcus faecalis / growth & development*
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Gentamicins / pharmacology
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Gram-Positive Bacterial Infections / drug therapy
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Gram-Positive Bacterial Infections / microbiology
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Humans
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Mutation
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N-Acetylmuramoyl-L-alanine Amidase / genetics
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N-Acetylmuramoyl-L-alanine Amidase / metabolism*
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Rabbits
Substances
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Anti-Bacterial Agents
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Gentamicins
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Amoxicillin
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N-Acetylmuramoyl-L-alanine Amidase