A carregar...
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...
Na minha lista:
| Main Authors: | , |
|---|---|
| Formato: | Artigo |
| Idioma: | en |
| Publicado em: |
American Society for Microbiology
2001
|
| Assuntos: | |
| 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 |
| Tags: |
Adicionar Tag
Sem tags, seja o primeiro a adicionar uma tag!
|
| id |
pubmed-98565 |
|---|---|
| record_format |
dspace |
| 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 |
| _version_ |
1759030608683597824 |