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Potential Virulence Role of the Legionella pneumophila ptsP Ortholog

We previously identified the Legionella pneumophila ptsP (phosphoenolpyruvate phosphotransferase) ortholog gene as a putative virulence factor in a study of signature-tagged mutagenesis using a guinea pig pneumonia model. In this study, we further defined the phenotypic properties of L. pneumophila...

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Main Authors: Higa, Futoshi, Edelstein, Paul H.
Formato: Artigo
Idioma:en
Publicado em: American Society for Microbiology 2001
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Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC98565/
https://ncbi.nlm.nih.gov/pubmed/11447151
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1128/IAI.69.8.4782-4789.2001
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spelling pubmed-985652002-09-12 Potential Virulence Role of the Legionella pneumophila ptsP Ortholog Higa, Futoshi Edelstein, Paul H. Infect Immun Bacterial Infections We previously identified the Legionella pneumophila ptsP (phosphoenolpyruvate phosphotransferase) ortholog gene as a putative virulence factor in a study of signature-tagged mutagenesis using a guinea pig pneumonia model. In this study, we further defined the phenotypic properties of L. pneumophila ptsP and its complete sequence. The L. pneumophila ptsP was 2,295 bases in length. Its deduced amino acid sequence had high similarity with ptsP orthologs of Pseudomonas aeruginosa, Azotobacter vinelandii, and Escherichia coli, with nearly identical lengths. Here we show that while the mutant grew well in laboratory media, it was defective in both lung and spleen multiplication in guinea pigs. It grew slowly in guinea pig alveolar macrophages despite good uptake into the cells. Furthermore, there was minimal growth in a human alveolar epithelial cell line (A549). Transcomplementation of the L. pneumophila ptsP mutant almost completely rescued its growth in alveolar macrophages, in A549 cells, and in guinea pig lung and spleen. The L. pneumophila ptsP mutant was capable of evasion of phagosome-lysosome fusion and resided in ribosome-studded phagosomes. Pore formation activity of the mutant was normal. The L. pneumophila ptsP mutant expressed DotA and IcmX in apparently normal amounts, suggesting that the ptsP mutation did not affect dotA and icmX regulation. In addition, the mutant was resistant to serum and neutrophil killing. Taken together, these findings show that L. pneumophila ptsP is required for full in vivo virulence of L. pneumophila, most probably by affecting intracellular growth. American Society for Microbiology 2001-08 /pmc/articles/PMC98565/ /pubmed/11447151 http://dx.doi.org/10.1128/IAI.69.8.4782-4789.2001 Text en Copyright © 2001, American Society for Microbiology
institution US National Library of Medicine
collection PubMed Central
language en
format Article
topic Bacterial Infections
spellingShingle Bacterial Infections
Higa, Futoshi
Edelstein, Paul H.
Potential Virulence Role of the Legionella pneumophila ptsP Ortholog
description We previously identified the Legionella pneumophila ptsP (phosphoenolpyruvate phosphotransferase) ortholog gene as a putative virulence factor in a study of signature-tagged mutagenesis using a guinea pig pneumonia model. In this study, we further defined the phenotypic properties of L. pneumophila ptsP and its complete sequence. The L. pneumophila ptsP was 2,295 bases in length. Its deduced amino acid sequence had high similarity with ptsP orthologs of Pseudomonas aeruginosa, Azotobacter vinelandii, and Escherichia coli, with nearly identical lengths. Here we show that while the mutant grew well in laboratory media, it was defective in both lung and spleen multiplication in guinea pigs. It grew slowly in guinea pig alveolar macrophages despite good uptake into the cells. Furthermore, there was minimal growth in a human alveolar epithelial cell line (A549). Transcomplementation of the L. pneumophila ptsP mutant almost completely rescued its growth in alveolar macrophages, in A549 cells, and in guinea pig lung and spleen. The L. pneumophila ptsP mutant was capable of evasion of phagosome-lysosome fusion and resided in ribosome-studded phagosomes. Pore formation activity of the mutant was normal. The L. pneumophila ptsP mutant expressed DotA and IcmX in apparently normal amounts, suggesting that the ptsP mutation did not affect dotA and icmX regulation. In addition, the mutant was resistant to serum and neutrophil killing. Taken together, these findings show that L. pneumophila ptsP is required for full in vivo virulence of L. pneumophila, most probably by affecting intracellular growth.
author Higa, Futoshi
Edelstein, Paul H.
author_facet Higa, Futoshi
Edelstein, Paul H.
author_sort Higa, Futoshi
title Potential Virulence Role of the Legionella pneumophila ptsP Ortholog
title_short Potential Virulence Role of the Legionella pneumophila ptsP Ortholog
title_full Potential Virulence Role of the Legionella pneumophila ptsP Ortholog
title_fullStr Potential Virulence Role of the Legionella pneumophila ptsP Ortholog
title_full_unstemmed Potential Virulence Role of the Legionella pneumophila ptsP Ortholog
title_sort potential virulence role of the legionella pneumophila ptsp ortholog
publisher American Society for Microbiology
publisher_facet American Society for Microbiology
publishDate 2001
url https://ncbi.nlm.nih.gov/pmc/articles/PMC98565/
https://ncbi.nlm.nih.gov/pubmed/11447151
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1128/IAI.69.8.4782-4789.2001
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