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The parasitic worm product ES-62 normalises the gut microbiota bone marrow axis in inflammatory arthritis

Author

Listed:
  • James Doonan

    (University of Strathclyde)

  • Anuradha Tarafdar

    (University of Glasgow)

  • Miguel A. Pineda

    (University of Glasgow)

  • Felicity E. Lumb

    (University of Strathclyde)

  • Jenny Crowe

    (University of Glasgow)

  • Aneesah M. Khan

    (University of Glasgow)

  • Paul A. Hoskisson

    (University of Strathclyde)

  • Margaret M. Harnett

    (University of Glasgow)

  • William Harnett

    (University of Strathclyde)

Abstract

The human immune system has evolved in the context of our colonisation by bacteria, viruses, fungi and parasitic helminths. Reflecting this, the rapid eradication of pathogens appears to have resulted in reduced microbiome diversity and generation of chronically activated immune systems, presaging the recent rise of allergic, autoimmune and metabolic disorders. Certainly, gastrointestinal helminths can protect against gut and lung mucosa inflammatory conditions by modulating the microbiome and suppressing the chronic inflammation associated with dysbiosis. Here, we employ ES-62, an immunomodulator secreted by tissue-dwelling Acanthocheilonema viteae to show that helminth-modulation of the gut microbiome does not require live infection with gastrointestinal-based worms nor is protection restricted to mucosal diseases. Specifically, subcutaneous administration of this defined immunomodulator affords protection against joint disease in collagen-induced arthritis, a mouse model of rheumatoid arthritis, which is associated with normalisation of gut microbiota and prevention of loss of intestinal barrier integrity.

Suggested Citation

  • James Doonan & Anuradha Tarafdar & Miguel A. Pineda & Felicity E. Lumb & Jenny Crowe & Aneesah M. Khan & Paul A. Hoskisson & Margaret M. Harnett & William Harnett, 2019. "The parasitic worm product ES-62 normalises the gut microbiota bone marrow axis in inflammatory arthritis," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-09361-0
    DOI: 10.1038/s41467-019-09361-0
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