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The dynamics of the human infant gut microbiome in development and in progression toward type 1 diabetes
Broad Institute of MIT and Harvard, Cambridge, MA, United States; Center for Computational and Integrative Bioogy, Massachusetts General Hospital, Harvard Medical School, Boston MA, United States; Department of Biostatistics, Harvard School of Public Health, Boston MA, United States.
Broad Institute of MIT and Harvard, Cambridge, MA, United States.
Department of Biostatistics, Harvard School of Public Health, Boston MA, United States; dChildren's Hospital, University of Helsinki, Helsinki University Hospital, Helsinki, Finland.
Broad Institute of MIT and Harvard, Cambridge, MA, United States; Department of Information and Computer Science, Aalto University School of Science, Espoo, Finland.
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2015 (English)In: Cell Host and Microbe, ISSN 1931-3128, E-ISSN 1934-6069, Vol. 17, no 2, p. 260-273, article id S1931-3128(15)00021-9Article in journal (Refereed) Published
Abstract [en]

Colonization of the fetal and infant gut microbiome results in dynamic changes in diversity, which can impact disease susceptibility. To examine the relationship between human gut microbiome dynamics throughout infancy and type 1 diabetes (T1D), we examined a cohort of 33 infants genetically predisposed to T1D. Modeling trajectories of microbial abundances through infancy revealed a subset of microbial relationships shared across most subjects. Although strain composition of a given species was highly variable between individuals, it was stable within individuals throughout infancy. Metabolic composition and metabolic pathway abundance remained constant across time. A marked drop in alpha-diversity was observed in T1D progressors in the time window between seroconversion and T1D diagnosis, accompanied by spikes in inflammation-favoring organisms, gene functions, and serum and stool metabolites. This work identifies trends in the development of the human infant gut microbiome along with specific alterations that precede T1D onset and distinguish T1D progressors from nonprogressors.

Place, publisher, year, edition, pages
Cell Press , 2015. Vol. 17, no 2, p. 260-273, article id S1931-3128(15)00021-9
National Category
Medical and Health Sciences Microbiology in the medical area
Identifiers
URN: urn:nbn:se:oru:diva-63703DOI: 10.1016/j.chom.2015.01.001ISI: 000349761700015PubMedID: 25662751Scopus ID: 2-s2.0-84922941772OAI: oai:DiVA.org:oru-63703DiVA, id: diva2:1169268
Funder
NIH (National Institute of Health), P30 DK043351 U54 DK102557
Note

Funding agencies:

European Union 202063 

Juvenile Diabetes Research Foundation 17-2011-529 17-2014-305 

Academy of Finland Centre of Excellence in Molecular Systems Immunology and Physiology Research 250114 

National Institutes of Health P30 DK043351 U54 DK102557

Available from: 2017-12-22 Created: 2017-12-22 Last updated: 2018-01-30Bibliographically approved

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Hyötyläinen, TuuliaOresic, Matej

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