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Changes in duodenal tissue-associated microbiota following hookworm infection and consecutive gluten challenges in humans with coeliac disease

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Giacomin, P 
Zakrzewski, M 
Jenkins, TP 
Su, X 
Al-Hallaf, R 


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.



Ancylostomatoidea, Animals, Bacteria, Celiac Disease, Duodenum, Feces, Humans, Microbiota, Sequence Analysis, DNA

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Scientific Reports

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Nature Publishing Group
Biotechnology and Biological Sciences Research Council (1643688)
This work was supported by grants 613718 to P.G., and 1037304 and 1020114 to A.L. from the National Health and Medical Research Council of Australia (NHMRC), and by the Royal Society and the Isaac Newton Trust/Wellcome Trust ISSF/University of Cambridge Joint Research Grants Scheme to C.C. T.J. is supported by scholarships from the Biotechnology and Biological Sciences Research Council (BBSRC) Doctoral Training Partnerships program.