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 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
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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.
container_issue 6
container_start_page 2345
container_title Infection and Immunity
container_volume 82
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