Analysis of Campylobacter jejuni infection in the gnotobiotic piglet and genome-wide identification of bacterial factors required for infection

Stefan P.W. de Vries; Aileen Linn; Kareen Macleod; Amanda MacCallum; Simon Hardy; Gill Douce; Eleanor Watson; Mark P. Dagleish; Hal Thompson; Andy Stevenson

doi:10.1038/srep44283

Analysis of Campylobacter jejuni infection in the gnotobiotic piglet and genome-wide identification of bacterial factors required for infection

Stefan P.W. de Vries, Aileen Linn, Kareen Macleod, Amanda MacCallum, Simon Hardy, Gill Douce, Eleanor Watson, Mark P. Dagleish, Hal Thompson, Andy Stevenson

University of Brighton

Research output: Contribution to journal › Article › peer-review

Abstract

To investigate how Campylobacter jejuni causes the clinical symptoms of diarrhoeal disease in humans,use of a relevant animal model is essential. Such a model should mimic the human disease closely in terms of host physiology, incubation period before onset of disease, clinical signs and a comparable outcome of disease. In this study, we used a gnotobiotic piglet model to study determinants of pathogenicity of C. jejuni. In this model, C. jejuni successfully established infection and piglets developed an increased temperature with watery diarrhoea, which was caused by a leaky epithelium and reduced bile re-absorption in the intestines. Further, we assessed the C. jejuni genes required for infection of the porcine gastrointestinal tract utilising a transposon (Tn) mutant library screen. A total of 123 genes of which Tn mutants showed attenuated piglet infection were identified. Our screen highlighted a crucial role for motility and chemotaxis, as well as central metabolism. In addition, Tn mutants of 14 genes displayed enhanced piglet infection. This study gives a unique insight into themechanisms of C. jejuni disease in terms of host physiology and contributing bacterial factors.

Original language	English
Journal	Scientific Reports
Volume	7
DOIs	https://doi.org/10.1038/srep44283
Publication status	Published - 10 Mar 2017

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title = "Analysis of Campylobacter jejuni infection in the gnotobiotic piglet and genome-wide identification of bacterial factors required for infection",

abstract = "To investigate how Campylobacter jejuni causes the clinical symptoms of diarrhoeal disease in humans,use of a relevant animal model is essential. Such a model should mimic the human disease closely in terms of host physiology, incubation period before onset of disease, clinical signs and a comparable outcome of disease. In this study, we used a gnotobiotic piglet model to study determinants of pathogenicity of C. jejuni. In this model, C. jejuni successfully established infection and piglets developed an increased temperature with watery diarrhoea, which was caused by a leaky epithelium and reduced bile re-absorption in the intestines. Further, we assessed the C. jejuni genes required for infection of the porcine gastrointestinal tract utilising a transposon (Tn) mutant library screen. A total of 123 genes of which Tn mutants showed attenuated piglet infection were identified. Our screen highlighted a crucial role for motility and chemotaxis, as well as central metabolism. In addition, Tn mutants of 14 genes displayed enhanced piglet infection. This study gives a unique insight into themechanisms of C. jejuni disease in terms of host physiology and contributing bacterial factors.",

author = "{de Vries}, {Stefan P.W.} and Aileen Linn and Kareen Macleod and Amanda MacCallum and Simon Hardy and Gill Douce and Eleanor Watson and Dagleish, {Mark P.} and Hal Thompson and Andy Stevenson",

note = "This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article{\textquoteright}s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/",

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AU - de Vries, Stefan P.W.

AU - Linn, Aileen

AU - Macleod, Kareen

AU - MacCallum, Amanda

AU - Hardy, Simon

AU - Douce, Gill

AU - Watson, Eleanor

AU - Dagleish, Mark P.

AU - Thompson, Hal

AU - Stevenson, Andy

N1 - This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

PY - 2017/3/10

Y1 - 2017/3/10

N2 - To investigate how Campylobacter jejuni causes the clinical symptoms of diarrhoeal disease in humans,use of a relevant animal model is essential. Such a model should mimic the human disease closely in terms of host physiology, incubation period before onset of disease, clinical signs and a comparable outcome of disease. In this study, we used a gnotobiotic piglet model to study determinants of pathogenicity of C. jejuni. In this model, C. jejuni successfully established infection and piglets developed an increased temperature with watery diarrhoea, which was caused by a leaky epithelium and reduced bile re-absorption in the intestines. Further, we assessed the C. jejuni genes required for infection of the porcine gastrointestinal tract utilising a transposon (Tn) mutant library screen. A total of 123 genes of which Tn mutants showed attenuated piglet infection were identified. Our screen highlighted a crucial role for motility and chemotaxis, as well as central metabolism. In addition, Tn mutants of 14 genes displayed enhanced piglet infection. This study gives a unique insight into themechanisms of C. jejuni disease in terms of host physiology and contributing bacterial factors.

AB - To investigate how Campylobacter jejuni causes the clinical symptoms of diarrhoeal disease in humans,use of a relevant animal model is essential. Such a model should mimic the human disease closely in terms of host physiology, incubation period before onset of disease, clinical signs and a comparable outcome of disease. In this study, we used a gnotobiotic piglet model to study determinants of pathogenicity of C. jejuni. In this model, C. jejuni successfully established infection and piglets developed an increased temperature with watery diarrhoea, which was caused by a leaky epithelium and reduced bile re-absorption in the intestines. Further, we assessed the C. jejuni genes required for infection of the porcine gastrointestinal tract utilising a transposon (Tn) mutant library screen. A total of 123 genes of which Tn mutants showed attenuated piglet infection were identified. Our screen highlighted a crucial role for motility and chemotaxis, as well as central metabolism. In addition, Tn mutants of 14 genes displayed enhanced piglet infection. This study gives a unique insight into themechanisms of C. jejuni disease in terms of host physiology and contributing bacterial factors.

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Analysis of Campylobacter jejuni infection in the gnotobiotic piglet and genome-wide identification of bacterial factors required for infection

Abstract

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