
Sandeep Gill
Doctor of Philosophy in Population and Public Health (PhD)
Research Topic
Examining the sinonasal microbiome and using a microbiome transplant as as potential treatment
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Human microbiome research and molecular epidemiology
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Background.Environmental enteric dysfunction (EED) is commonly defined as an acquired subclinicaldisorder of the small intestine, characterized by villous atrophy and crypt hyperplasia. EED hasbeen proposed to underlie stunted growth among children in developing countries. A collectionof biomarkers, organized into distinct domains, has been used to measure different aspects ofEED. Here, we examine whether these hypothesized relationships, among EED domains andbetween each domain and stunting, are supported by data from recent studies.Methodology.A systematic literature search was conducted using PubMed, MEDLINE, EMBASE, Web ofScience, and CINAHL between January 1, 2010 and April 20, 2017. Information on studyobjective, design, population, location, biomarkers, and results were recorded, as well asqualitative and quantitative definitions of EED. Biomarkers were organized into five EEDdomains, and the number of studies that support or do not support relationships among domainsand between each domain with stunting were summarized.Results.There was little evidence to support the pathway from intestinal permeability to microbialtranslocation and from microbial translocation to stunting, but stronger support existed for thelink between intestinal inflammation and systemic inflammation and for intestinal inflammationand stunting. There was conflicting evidence for the pathways from intestinal damage tointestinal permeability and intestinal damage to stunting.Conclusions.These results suggest that certain EED biomarkers may require reconsideration, particularlythose most difficult to measure, such as microbial translocation and intestinal permeability. Wediscuss several issues with currently used biomarkers and recommend further analysis ofpathogen-induced changes to the intestinal microbiota as a pathway leading to stunting.
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