Abstract
Pseudomonas aeruginosa infection is preceded by selective adhesion of the bacteria to the host target cells via diverse adhesins, including lectins. This step enables maximal damage to the target host cells by the bacterially secreted injurious toxins and enzymes. The production of both lectins and many of the virulence factors is positively controlled by transcription activators including signaling autoinducers (N-acyl-L-homoserine lactones). We show in this communication that erythromycin at subminimal growth inhibitory concentrations simultaneously suppresses the production of P. aeruginosa hemagglutinins (including lectins), protease, hemolysin and homoserine lactone autoinducers. The antibiotic-treated bacteria also show reduced virulence to mice, endorsing clinical observations that indicate the efficiency of low-dose erythromycin treatment of persistent drug-resistant P. aeruginosa infections.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adhesins, Bacterial / biosynthesis*
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Adhesins, Bacterial / drug effects
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Animals
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Anti-Bacterial Agents / pharmacology
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Bacterial Adhesion / drug effects
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Dose-Response Relationship, Drug
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Drug Resistance, Microbial
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Erythromycin / pharmacology*
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Extracellular Matrix / drug effects
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Extracellular Matrix / metabolism
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Hemagglutination Tests
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Homoserine / analogs & derivatives*
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Homoserine / drug effects
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Homoserine / metabolism
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Humans
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Lactones / metabolism*
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Lectins*
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Mice
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Mice, Inbred ICR
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Microbial Sensitivity Tests
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Protein Synthesis Inhibitors / pharmacology*
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Pseudomonas aeruginosa / drug effects*
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Pseudomonas aeruginosa / metabolism
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Pseudomonas aeruginosa / pathogenicity
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Virulence / drug effects
Substances
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Adhesins, Bacterial
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Anti-Bacterial Agents
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Lactones
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Lectins
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Protein Synthesis Inhibitors
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adhesin, Pseudomonas
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Pseudomonas aeruginosa autoinducer
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Erythromycin
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Homoserine