Abstract
Cell-to-cell signaling controls many virulence genes in Pseudomonas aeruginosa. We tested the virulence of las and rhl quorum-sensing mutants in neonatal mice. A lasI rhlI double mutant was nearly avirulent, and the respective single mutant strains were reduced in virulence compared with the wild-type strain. Quorum sensing plays a role in P. aeruginosa pneumonia in neonatal mice.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Animals, Newborn
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Bacterial Proteins / genetics
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Bacterial Proteins / physiology
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Disease Models, Animal
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Genes, Bacterial
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Ligases
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Mice
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Mice, Inbred BALB C
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Mutation
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Pneumonia, Bacterial / etiology*
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Pneumonia, Bacterial / microbiology
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Pneumonia, Bacterial / pathology
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Pseudomonas Infections / etiology*
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Pseudomonas Infections / microbiology
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Pseudomonas Infections / pathology
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Pseudomonas aeruginosa / genetics
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Pseudomonas aeruginosa / pathogenicity*
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Pseudomonas aeruginosa / physiology*
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Signal Transduction
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Transcription Factors / genetics
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Transcription Factors / physiology
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Virulence / genetics
Substances
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Bacterial Proteins
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LasI protein, Pseudomonas aeruginosa
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Transcription Factors
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Ligases
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RHLI protein, Pseudomonas aeruginosa