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Experimental hookworm infection and escalating gluten challenges are associated with increased microbial richness in celiac subjects.


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Authors

Giacomin, Paul 
Zakrzewski, Martha 
Croese, John 
Su, Xiaopei 
Sotillo, Javier 

Abstract

The intestinal microbiota plays a critical role in the development of the immune system. Recent investigations have highlighted the potential of helminth therapy for treating a range of inflammatory disorders, including celiac disease (CeD); however, the mechanisms by which helminths modulate the immune response of the human host and ameliorate CeD pathology are unknown. In this study, we investigated the potential role of alterations in the human gut microbiota in helminth-mediated suppression of an inflammatory disease. We assessed the qualitative and quantitative changes in the microbiota of human volunteers with CeD prior to and following infection with human hookworms, and following challenge with escalating doses of dietary gluten. Experimental hookworm infection of the trial subjects resulted in maintenance of the composition of the intestinal flora, even after a moderate gluten challenge. Notably, we observed a significant increase in microbial species richness over the course of the trial, which could represent a potential mechanism by which hookworms can regulate gluten-induced inflammation and maintain intestinal immune homeostasis.

Description

Keywords

Ancylostomatoidea, Animals, Biodiversity, Case-Control Studies, Celiac Disease, Feces, Gastrointestinal Microbiome, Glutens, High-Throughput Nucleotide Sequencing, Hookworm Infections, Humans, Immunomodulation, Metagenome, Metagenomics

Journal Title

Sci Rep

Conference Name

Journal ISSN

2045-2322
2045-2322

Volume Title

5

Publisher

Springer Science and Business Media LLC
Sponsorship
This work was supported by grants 1052938 to C.C., 613718 to P.G., and 1037304 and 1020114 to A.L. from the National Health and Medical Research Council of Australia (NHMRC), and from James Cook University (FMHMS 2013 grants round) and the Isaac Newton Trust / Wellcome Trust ISSF / University of Cambridge Joint Research Grants Scheme to C.C.