Changes in duodenal tissue-associated microbiota following hookworm infection and consecutive gluten challenges in humans with coeliac disease
Web of Science
AuthorGiacomin, P; Zakrzewski, M; Jenkins, TP; Su, X; Al-Hallaf, R; Croese, J; de Vries, S; Grant, A; Mitreva, M; Loukas, A; ...
Source TitleScientific Reports
PublisherNATURE PUBLISHING GROUP
University of Melbourne Author/sCantacessi, Cinzia
Document TypeJournal Article
CitationsGiacomin, P., Zakrzewski, M., Jenkins, T. P., Su, X., Al-Hallaf, R., Croese, J., de Vries, S., Grant, A., Mitreva, M., Loukas, A., Krause, L. & Cantacessi, C. (2016). Changes in duodenal tissue-associated microbiota following hookworm infection and consecutive gluten challenges in humans with coeliac disease. SCIENTIFIC REPORTS, 6 (1), https://doi.org/10.1038/srep36797.
Access StatusOpen Access
A reduced diversity of the gastrointestinal commensal microbiota is associated with the development of several inflammatory diseases. Recent reports in humans and animal models have demonstrated the beneficial therapeutic effects of infections by parasitic worms (helminths) in some inflammatory disorders, such as inflammatory bowel disease (IBD) and coeliac disease (CeD). Interestingly, these studies have described how helminths may alter the intestinal microbiota, potentially representing a mechanism by which they regulate inflammation. However, for practical reasons, these reports have primarily analysed the faecal microbiota. In the present investigation, we have assessed, for the first time, the changes in the microbiota at the site of infection by a parasitic helminth (hookworm) and gluten-dependent inflammation in humans with CeD using biopsy tissue from the duodenum. Hookworm infection and gluten exposure were associated with an increased abundance of species within the Bacteroides phylum, as well as increases in the richness and diversity of the tissue-resident microbiota within the intestine, results that are consistent with previous reports using other helminth species in humans and animal models. Hence, this may represent a mechanism by which parasitic helminths may restore intestinal immune homeostasis and exert a therapeutic benefit in CeD, and potentially other inflammatory disorders.
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