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The role of toxin A and toxin B in Clostridium difficile infection

Author

Listed:
  • Sarah A. Kuehne

    (Clostridia Research Group, Centre for Biomolecular Sciences, School of Molecular Medical Sciences, Nottingham Digestive Diseases Centre, NIHR Biomedical Research Unit, University of Nottingham)

  • Stephen T. Cartman

    (Clostridia Research Group, Centre for Biomolecular Sciences, School of Molecular Medical Sciences, Nottingham Digestive Diseases Centre, NIHR Biomedical Research Unit, University of Nottingham)

  • John T. Heap

    (Clostridia Research Group, Centre for Biomolecular Sciences, School of Molecular Medical Sciences, Nottingham Digestive Diseases Centre, NIHR Biomedical Research Unit, University of Nottingham)

  • Michelle L. Kelly

    (Clostridia Research Group, Centre for Biomolecular Sciences, School of Molecular Medical Sciences, Nottingham Digestive Diseases Centre, NIHR Biomedical Research Unit, University of Nottingham)

  • Alan Cockayne

    (Clostridia Research Group, Centre for Biomolecular Sciences, School of Molecular Medical Sciences, Nottingham Digestive Diseases Centre, NIHR Biomedical Research Unit, University of Nottingham)

  • Nigel P. Minton

    (Clostridia Research Group, Centre for Biomolecular Sciences, School of Molecular Medical Sciences, Nottingham Digestive Diseases Centre, NIHR Biomedical Research Unit, University of Nottingham)

Abstract

Clostridium difficile toxins revisited Clostridium difficile, the most common cause of infectious diarrhoea in hospitals in Europe and North America, produces two toxins. Their relative importance has been widely debated, and although animal studies had indicated that purified toxin A alone can induce most of the pathology observed in C. difficile infections, a recent Nature paper ( http://go.nature.com/oh6un5 ) suggested that the other toxin, toxin B, was the main cause of disease symptoms. Now a new study, involving C. difficile strains producing either toxin A or toxin B alone and — for the first time — a double-mutant strain producing neither, demonstrates that both toxins are important for disease, and need to be considered for diagnosis and treatment.

Suggested Citation

  • Sarah A. Kuehne & Stephen T. Cartman & John T. Heap & Michelle L. Kelly & Alan Cockayne & Nigel P. Minton, 2010. "The role of toxin A and toxin B in Clostridium difficile infection," Nature, Nature, vol. 467(7316), pages 711-713, October.
    • Handle: RePEc:nat:nature:v:467:y:2010:i:7316:d:10.1038_nature09397
    DOI: 10.1038/nature09397
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    Cited by:

    1. Songhai Tian & Xiaozhe Xiong & Ji Zeng & Siyu Wang & Benjamin Jean-Marie Tremblay & Peng Chen & Baohua Chen & Min Liu & Pengsheng Chen & Kuanwei Sheng & Daniel Zeve & Wanshu Qi & David T. Breault & Cé, 2022. "Identification of TFPI as a receptor reveals recombination-driven receptor switching in Clostridioides difficile toxin B variants," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    2. Xinchen Lv & Yuanyuan Zhang & Ke Sun & Qi Yang & Jianhua Luo & Liang Tao & Peilong Lu, 2024. "De novo design of mini-protein binders broadly neutralizing Clostridioides difficile toxin B variants," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    3. Lola Rueda Ruzafa & José Luis Cedillo & Arik J. Hone, 2021. "Nicotinic Acetylcholine Receptor Involvement in Inflammatory Bowel Disease and Interactions with Gut Microbiota," IJERPH, MDPI, vol. 18(3), pages 1-19, January.
    4. Ashleigh S. Paparella & Briana L. Aboulache & Rajesh K. Harijan & Kathryn S. Potts & Peter C. Tyler & Vern L. Schramm, 2021. "Inhibition of Clostridium difficile TcdA and TcdB toxins with transition state analogues," Nature Communications, Nature, vol. 12(1), pages 1-13, December.

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