Chemotherapy · 1999 · 87 citations · 17 references
Life SciencesInfectious DiseasesMicrobiologyHost-pathogen InteractionsMicrobial PathogenesisSignal TransductionAntibiotic ResistanceBacterial Gene RegulationBacterial PathogenesisBacterial Virulence FactorsMicrobial Virulence FactorsVirulence Gene RegulationLectin-mediated AttachmentLectin-mediated Microbial InteractionsLectin-mediated SignalingMicrobial LectinsN-acyl Homoserine LactonesPseudomonas Aeruginosa ResistanceTranscriptional ActivatorsVirulence Determinants
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.
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Michael K. Winson, Miguel Cámara, Amel Latifi et al. · Proceedings of the National Academy of Sciences · 1995 · 538 citations · Full text