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Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection...
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Zeitschriftentitel: | Infection and Immunity |
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Personen und Körperschaften: | , , , , , |
In: | Infection and Immunity, 82, 2014, 6, S. 2345-2355 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
American Society for Microbiology
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author_facet |
Ho, Theresa D. Williams, Kyle B. Chen, Yan Helm, Richard F. Popham, David L. Ellermeier, Craig D. Ho, Theresa D. Williams, Kyle B. Chen, Yan Helm, Richard F. Popham, David L. Ellermeier, Craig D. |
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author |
Ho, Theresa D. Williams, Kyle B. Chen, Yan Helm, Richard F. Popham, David L. Ellermeier, Craig D. |
spellingShingle |
Ho, Theresa D. Williams, Kyle B. Chen, Yan Helm, Richard F. Popham, David L. Ellermeier, Craig D. Infection and Immunity Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection Infectious Diseases Immunology Microbiology Parasitology |
author_sort |
ho, theresa d. |
spelling |
Ho, Theresa D. Williams, Kyle B. Chen, Yan Helm, Richard F. Popham, David L. Ellermeier, Craig D. 0019-9567 1098-5522 American Society for Microbiology Infectious Diseases Immunology Microbiology Parasitology http://dx.doi.org/10.1128/iai.01483-13 <jats:title>ABSTRACT</jats:title> <jats:p> <jats:named-content content-type="genus-species">Clostridium difficile</jats:named-content> is a clinically important pathogen and the most common cause of hospital-acquired infectious diarrhea. Expression of the <jats:named-content content-type="genus-species">C. difficile</jats:named-content> gene <jats:italic>csfV</jats:italic> , which encodes σ <jats:sup>V</jats:sup> , an extracytoplasmic function σ factor, is induced by lysozyme, which damages the peptidoglycan of bacteria. Here we show that σ <jats:sup>V</jats:sup> is required for lysozyme resistance in <jats:named-content content-type="genus-species">C. difficile</jats:named-content> . Using microarray analysis, we identified the <jats:named-content content-type="genus-species">C. difficile</jats:named-content> genes whose expression is dependent upon σ <jats:sup>V</jats:sup> and is induced by lysozyme. Although the peptidoglycan of wild-type <jats:named-content content-type="genus-species">C. difficile</jats:named-content> is intrinsically highly deacetylated, we have found that exposure to lysozyme leads to additional peptidoglycan deacetylation. This lysozyme-induced deacetylation is dependent upon σ <jats:sup>V</jats:sup> . Expression of <jats:italic>pdaV</jats:italic> , which encodes a putative peptidoglycan deacetylase, was able to increase lysozyme resistance of a <jats:italic>csfV</jats:italic> mutant. The <jats:italic>csfV</jats:italic> mutant strain is severely attenuated compared to wild-type <jats:named-content content-type="genus-species">C. difficile</jats:named-content> in a hamster model of <jats:named-content content-type="genus-species">C. difficile</jats:named-content> -associated disease. We conclude that the σ <jats:sup>V</jats:sup> signal transduction system, which senses the host innate immune defense enzyme lysozyme, is required for lysozyme resistance and is necessary during <jats:named-content content-type="genus-species">C. difficile</jats:named-content> infection. </jats:p> Clostridium difficile Extracytoplasmic Function σ Factor σ <sup>V</sup> Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection Infection and Immunity |
doi_str_mv |
10.1128/iai.01483-13 |
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Medizin Biologie |
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American Society for Microbiology, 2014 |
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American Society for Microbiology, 2014 |
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2014 |
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American Society for Microbiology |
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Infection and Immunity |
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title |
Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_unstemmed |
Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_full |
Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_fullStr |
Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_full_unstemmed |
Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_short |
Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_sort |
clostridium difficile extracytoplasmic function σ factor σ
<sup>v</sup>
regulates lysozyme resistance and is necessary for pathogenesis in the hamster model of infection |
topic |
Infectious Diseases Immunology Microbiology Parasitology |
url |
http://dx.doi.org/10.1128/iai.01483-13 |
publishDate |
2014 |
physical |
2345-2355 |
description |
<jats:title>ABSTRACT</jats:title>
<jats:p>
<jats:named-content content-type="genus-species">Clostridium difficile</jats:named-content>
is a clinically important pathogen and the most common cause of hospital-acquired infectious diarrhea. Expression of the
<jats:named-content content-type="genus-species">C. difficile</jats:named-content>
gene
<jats:italic>csfV</jats:italic>
, which encodes σ
<jats:sup>V</jats:sup>
, an extracytoplasmic function σ factor, is induced by lysozyme, which damages the peptidoglycan of bacteria. Here we show that σ
<jats:sup>V</jats:sup>
is required for lysozyme resistance in
<jats:named-content content-type="genus-species">C. difficile</jats:named-content>
. Using microarray analysis, we identified the
<jats:named-content content-type="genus-species">C. difficile</jats:named-content>
genes whose expression is dependent upon σ
<jats:sup>V</jats:sup>
and is induced by lysozyme. Although the peptidoglycan of wild-type
<jats:named-content content-type="genus-species">C. difficile</jats:named-content>
is intrinsically highly deacetylated, we have found that exposure to lysozyme leads to additional peptidoglycan deacetylation. This lysozyme-induced deacetylation is dependent upon σ
<jats:sup>V</jats:sup>
. Expression of
<jats:italic>pdaV</jats:italic>
, which encodes a putative peptidoglycan deacetylase, was able to increase lysozyme resistance of a
<jats:italic>csfV</jats:italic>
mutant. The
<jats:italic>csfV</jats:italic>
mutant strain is severely attenuated compared to wild-type
<jats:named-content content-type="genus-species">C. difficile</jats:named-content>
in a hamster model of
<jats:named-content content-type="genus-species">C. difficile</jats:named-content>
-associated disease. We conclude that the σ
<jats:sup>V</jats:sup>
signal transduction system, which senses the host innate immune defense enzyme lysozyme, is required for lysozyme resistance and is necessary during
<jats:named-content content-type="genus-species">C. difficile</jats:named-content>
infection.
</jats:p> |
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author | Ho, Theresa D., Williams, Kyle B., Chen, Yan, Helm, Richard F., Popham, David L., Ellermeier, Craig D. |
author_facet | Ho, Theresa D., Williams, Kyle B., Chen, Yan, Helm, Richard F., Popham, David L., Ellermeier, Craig D., Ho, Theresa D., Williams, Kyle B., Chen, Yan, Helm, Richard F., Popham, David L., Ellermeier, Craig D. |
author_sort | ho, theresa d. |
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description | <jats:title>ABSTRACT</jats:title> <jats:p> <jats:named-content content-type="genus-species">Clostridium difficile</jats:named-content> is a clinically important pathogen and the most common cause of hospital-acquired infectious diarrhea. Expression of the <jats:named-content content-type="genus-species">C. difficile</jats:named-content> gene <jats:italic>csfV</jats:italic> , which encodes σ <jats:sup>V</jats:sup> , an extracytoplasmic function σ factor, is induced by lysozyme, which damages the peptidoglycan of bacteria. Here we show that σ <jats:sup>V</jats:sup> is required for lysozyme resistance in <jats:named-content content-type="genus-species">C. difficile</jats:named-content> . Using microarray analysis, we identified the <jats:named-content content-type="genus-species">C. difficile</jats:named-content> genes whose expression is dependent upon σ <jats:sup>V</jats:sup> and is induced by lysozyme. Although the peptidoglycan of wild-type <jats:named-content content-type="genus-species">C. difficile</jats:named-content> is intrinsically highly deacetylated, we have found that exposure to lysozyme leads to additional peptidoglycan deacetylation. This lysozyme-induced deacetylation is dependent upon σ <jats:sup>V</jats:sup> . Expression of <jats:italic>pdaV</jats:italic> , which encodes a putative peptidoglycan deacetylase, was able to increase lysozyme resistance of a <jats:italic>csfV</jats:italic> mutant. The <jats:italic>csfV</jats:italic> mutant strain is severely attenuated compared to wild-type <jats:named-content content-type="genus-species">C. difficile</jats:named-content> in a hamster model of <jats:named-content content-type="genus-species">C. difficile</jats:named-content> -associated disease. We conclude that the σ <jats:sup>V</jats:sup> signal transduction system, which senses the host innate immune defense enzyme lysozyme, is required for lysozyme resistance and is necessary during <jats:named-content content-type="genus-species">C. difficile</jats:named-content> infection. </jats:p> |
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spelling | Ho, Theresa D. Williams, Kyle B. Chen, Yan Helm, Richard F. Popham, David L. Ellermeier, Craig D. 0019-9567 1098-5522 American Society for Microbiology Infectious Diseases Immunology Microbiology Parasitology http://dx.doi.org/10.1128/iai.01483-13 <jats:title>ABSTRACT</jats:title> <jats:p> <jats:named-content content-type="genus-species">Clostridium difficile</jats:named-content> is a clinically important pathogen and the most common cause of hospital-acquired infectious diarrhea. Expression of the <jats:named-content content-type="genus-species">C. difficile</jats:named-content> gene <jats:italic>csfV</jats:italic> , which encodes σ <jats:sup>V</jats:sup> , an extracytoplasmic function σ factor, is induced by lysozyme, which damages the peptidoglycan of bacteria. Here we show that σ <jats:sup>V</jats:sup> is required for lysozyme resistance in <jats:named-content content-type="genus-species">C. difficile</jats:named-content> . Using microarray analysis, we identified the <jats:named-content content-type="genus-species">C. difficile</jats:named-content> genes whose expression is dependent upon σ <jats:sup>V</jats:sup> and is induced by lysozyme. Although the peptidoglycan of wild-type <jats:named-content content-type="genus-species">C. difficile</jats:named-content> is intrinsically highly deacetylated, we have found that exposure to lysozyme leads to additional peptidoglycan deacetylation. This lysozyme-induced deacetylation is dependent upon σ <jats:sup>V</jats:sup> . Expression of <jats:italic>pdaV</jats:italic> , which encodes a putative peptidoglycan deacetylase, was able to increase lysozyme resistance of a <jats:italic>csfV</jats:italic> mutant. The <jats:italic>csfV</jats:italic> mutant strain is severely attenuated compared to wild-type <jats:named-content content-type="genus-species">C. difficile</jats:named-content> in a hamster model of <jats:named-content content-type="genus-species">C. difficile</jats:named-content> -associated disease. We conclude that the σ <jats:sup>V</jats:sup> signal transduction system, which senses the host innate immune defense enzyme lysozyme, is required for lysozyme resistance and is necessary during <jats:named-content content-type="genus-species">C. difficile</jats:named-content> infection. </jats:p> Clostridium difficile Extracytoplasmic Function σ Factor σ <sup>V</sup> Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection Infection and Immunity |
spellingShingle | Ho, Theresa D., Williams, Kyle B., Chen, Yan, Helm, Richard F., Popham, David L., Ellermeier, Craig D., Infection and Immunity, Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection, Infectious Diseases, Immunology, Microbiology, Parasitology |
title | Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_full | Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_fullStr | Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_full_unstemmed | Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_short | Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
title_sort | clostridium difficile extracytoplasmic function σ factor σ <sup>v</sup> regulates lysozyme resistance and is necessary for pathogenesis in the hamster model of infection |
title_unstemmed | Clostridium difficile Extracytoplasmic Function σ Factor σ V Regulates Lysozyme Resistance and Is Necessary for Pathogenesis in the Hamster Model of Infection |
topic | Infectious Diseases, Immunology, Microbiology, Parasitology |
url | http://dx.doi.org/10.1128/iai.01483-13 |