Growth of <it<Yersinia pseudotuberculosis </it<in human plasma: impacts on virulence and metabolic gene expression
<p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the diges...
Ausführliche Beschreibung
Autor*in: |
Coppée Jean-Yves [verfasserIn] Foulon Jeannine [verfasserIn] Dillies Marie-Agnès [verfasserIn] Schiavo Angèle [verfasserIn] Lacroix Céline [verfasserIn] Frangeul Lionel [verfasserIn] Laurans Caroline [verfasserIn] Chauvaux Sylvie [verfasserIn] Dessein Rodrigue [verfasserIn] Rosso Marie-Laure [verfasserIn] Médigue Claudine [verfasserIn] Carniel Elisabeth [verfasserIn] Simonet Michel [verfasserIn] Marceau Michaël [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2008 |
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Übergeordnetes Werk: |
In: BMC Microbiology - BMC, 2003, 8(2008), 1, p 211 |
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Übergeordnetes Werk: |
volume:8 ; year:2008 ; number:1, p 211 |
Links: |
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DOI / URN: |
10.1186/1471-2180-8-211 |
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Katalog-ID: |
DOAJ00747430X |
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520 | |a <p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< | ||
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700 | 0 | |a Dillies Marie-Agnès |e verfasserin |4 aut | |
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700 | 0 | |a Simonet Michel |e verfasserin |4 aut | |
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10.1186/1471-2180-8-211 doi (DE-627)DOAJ00747430X (DE-599)DOAJ0de1420a834845b0a1f2077e90bd70de DE-627 ger DE-627 rakwb eng QR1-502 Coppée Jean-Yves verfasserin aut Growth of <it<Yersinia pseudotuberculosis </it<in human plasma: impacts on virulence and metabolic gene expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< Microbiology Foulon Jeannine verfasserin aut Dillies Marie-Agnès verfasserin aut Schiavo Angèle verfasserin aut Lacroix Céline verfasserin aut Frangeul Lionel verfasserin aut Laurans Caroline verfasserin aut Chauvaux Sylvie verfasserin aut Dessein Rodrigue verfasserin aut Rosso Marie-Laure verfasserin aut Médigue Claudine verfasserin aut Carniel Elisabeth verfasserin aut Simonet Michel verfasserin aut Marceau Michaël verfasserin aut In BMC Microbiology BMC, 2003 8(2008), 1, p 211 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:8 year:2008 number:1, p 211 https://doi.org/10.1186/1471-2180-8-211 kostenfrei https://doaj.org/article/0de1420a834845b0a1f2077e90bd70de kostenfrei http://www.biomedcentral.com/1471-2180/8/211 kostenfrei https://doaj.org/toc/1471-2180 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2008 1, p 211 |
spelling |
10.1186/1471-2180-8-211 doi (DE-627)DOAJ00747430X (DE-599)DOAJ0de1420a834845b0a1f2077e90bd70de DE-627 ger DE-627 rakwb eng QR1-502 Coppée Jean-Yves verfasserin aut Growth of <it<Yersinia pseudotuberculosis </it<in human plasma: impacts on virulence and metabolic gene expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< Microbiology Foulon Jeannine verfasserin aut Dillies Marie-Agnès verfasserin aut Schiavo Angèle verfasserin aut Lacroix Céline verfasserin aut Frangeul Lionel verfasserin aut Laurans Caroline verfasserin aut Chauvaux Sylvie verfasserin aut Dessein Rodrigue verfasserin aut Rosso Marie-Laure verfasserin aut Médigue Claudine verfasserin aut Carniel Elisabeth verfasserin aut Simonet Michel verfasserin aut Marceau Michaël verfasserin aut In BMC Microbiology BMC, 2003 8(2008), 1, p 211 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:8 year:2008 number:1, p 211 https://doi.org/10.1186/1471-2180-8-211 kostenfrei https://doaj.org/article/0de1420a834845b0a1f2077e90bd70de kostenfrei http://www.biomedcentral.com/1471-2180/8/211 kostenfrei https://doaj.org/toc/1471-2180 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2008 1, p 211 |
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10.1186/1471-2180-8-211 doi (DE-627)DOAJ00747430X (DE-599)DOAJ0de1420a834845b0a1f2077e90bd70de DE-627 ger DE-627 rakwb eng QR1-502 Coppée Jean-Yves verfasserin aut Growth of <it<Yersinia pseudotuberculosis </it<in human plasma: impacts on virulence and metabolic gene expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< Microbiology Foulon Jeannine verfasserin aut Dillies Marie-Agnès verfasserin aut Schiavo Angèle verfasserin aut Lacroix Céline verfasserin aut Frangeul Lionel verfasserin aut Laurans Caroline verfasserin aut Chauvaux Sylvie verfasserin aut Dessein Rodrigue verfasserin aut Rosso Marie-Laure verfasserin aut Médigue Claudine verfasserin aut Carniel Elisabeth verfasserin aut Simonet Michel verfasserin aut Marceau Michaël verfasserin aut In BMC Microbiology BMC, 2003 8(2008), 1, p 211 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:8 year:2008 number:1, p 211 https://doi.org/10.1186/1471-2180-8-211 kostenfrei https://doaj.org/article/0de1420a834845b0a1f2077e90bd70de kostenfrei http://www.biomedcentral.com/1471-2180/8/211 kostenfrei https://doaj.org/toc/1471-2180 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2008 1, p 211 |
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10.1186/1471-2180-8-211 doi (DE-627)DOAJ00747430X (DE-599)DOAJ0de1420a834845b0a1f2077e90bd70de DE-627 ger DE-627 rakwb eng QR1-502 Coppée Jean-Yves verfasserin aut Growth of <it<Yersinia pseudotuberculosis </it<in human plasma: impacts on virulence and metabolic gene expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< Microbiology Foulon Jeannine verfasserin aut Dillies Marie-Agnès verfasserin aut Schiavo Angèle verfasserin aut Lacroix Céline verfasserin aut Frangeul Lionel verfasserin aut Laurans Caroline verfasserin aut Chauvaux Sylvie verfasserin aut Dessein Rodrigue verfasserin aut Rosso Marie-Laure verfasserin aut Médigue Claudine verfasserin aut Carniel Elisabeth verfasserin aut Simonet Michel verfasserin aut Marceau Michaël verfasserin aut In BMC Microbiology BMC, 2003 8(2008), 1, p 211 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:8 year:2008 number:1, p 211 https://doi.org/10.1186/1471-2180-8-211 kostenfrei https://doaj.org/article/0de1420a834845b0a1f2077e90bd70de kostenfrei http://www.biomedcentral.com/1471-2180/8/211 kostenfrei https://doaj.org/toc/1471-2180 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2008 1, p 211 |
allfieldsSound |
10.1186/1471-2180-8-211 doi (DE-627)DOAJ00747430X (DE-599)DOAJ0de1420a834845b0a1f2077e90bd70de DE-627 ger DE-627 rakwb eng QR1-502 Coppée Jean-Yves verfasserin aut Growth of <it<Yersinia pseudotuberculosis </it<in human plasma: impacts on virulence and metabolic gene expression 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< Microbiology Foulon Jeannine verfasserin aut Dillies Marie-Agnès verfasserin aut Schiavo Angèle verfasserin aut Lacroix Céline verfasserin aut Frangeul Lionel verfasserin aut Laurans Caroline verfasserin aut Chauvaux Sylvie verfasserin aut Dessein Rodrigue verfasserin aut Rosso Marie-Laure verfasserin aut Médigue Claudine verfasserin aut Carniel Elisabeth verfasserin aut Simonet Michel verfasserin aut Marceau Michaël verfasserin aut In BMC Microbiology BMC, 2003 8(2008), 1, p 211 (DE-627)326644997 (DE-600)2041505-9 14712180 nnns volume:8 year:2008 number:1, p 211 https://doi.org/10.1186/1471-2180-8-211 kostenfrei https://doaj.org/article/0de1420a834845b0a1f2077e90bd70de kostenfrei http://www.biomedcentral.com/1471-2180/8/211 kostenfrei https://doaj.org/toc/1471-2180 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2008 1, p 211 |
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Coppée Jean-Yves @@aut@@ Foulon Jeannine @@aut@@ Dillies Marie-Agnès @@aut@@ Schiavo Angèle @@aut@@ Lacroix Céline @@aut@@ Frangeul Lionel @@aut@@ Laurans Caroline @@aut@@ Chauvaux Sylvie @@aut@@ Dessein Rodrigue @@aut@@ Rosso Marie-Laure @@aut@@ Médigue Claudine @@aut@@ Carniel Elisabeth @@aut@@ Simonet Michel @@aut@@ Marceau Michaël @@aut@@ |
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growth of <it<yersinia pseudotuberculosis </it<in human plasma: impacts on virulence and metabolic gene expression |
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Growth of <it<Yersinia pseudotuberculosis </it<in human plasma: impacts on virulence and metabolic gene expression |
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<p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< |
abstractGer |
<p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< |
abstract_unstemmed |
<p<Abstract</p< <p<Background</p< <p<In man, infection by the Gram-negative enteropathogen <it<Yersinia pseudotuberculosis </it<is usually limited to the terminal ileum. However, in immunocompromised patients, the microorganism may disseminate from the digestive tract and thus cause a systemic infection with septicemia.</p< <p<Results</p< <p<To gain insight into the metabolic pathways and virulence factors expressed by the bacterium at the blood stage of pseudotuberculosis, we compared the overall gene transcription patterns (the transcriptome) of bacterial cells cultured in either human plasma or Luria-Bertani medium. The most marked plasma-triggered metabolic consequence in <it<Y. pseudotuberculosis </it<was the switch to high glucose consumption, which is reminiscent of the acetogenic pathway (known as "glucose overflow") in <it<Escherichia coli</it<. However, upregulation of the glyoxylate shunt enzymes suggests that (in contrast to <it<E. coli</it<) acetate may be further metabolized in <it<Y. pseudotuberculosis</it<. Our data also indicate that the bloodstream environment can regulate major virulence genes (positively or negatively); the <it<yadA </it<adhesin gene and most of the transcriptional units of the pYV-encoded type III secretion apparatus were found to be upregulated, whereas transcription of the pH6 antigen locus was strongly repressed.</p< <p<Conclusion</p< <p<Our results suggest that plasma growth of <it<Y. pseudotuberculosis </it<is responsible for major transcriptional regulatory events and prompts key metabolic reorientations within the bacterium, which may in turn have an impact on virulence.</p< |
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