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Compromised gut microbiota networks in children with anti-islet cell autoimmunity.

Abstract

The gut microbiome is suggested to play a role in the pathogenesis of autoimmune disorders such as type 1 diabetes. Evidence of anti-islet cell autoimmunity in type 1 diabetes appears in the first years of life; however, little is known regarding the establishment of the gut microbiome in early infancy. Here, we sought to determine whether differences were present in early composition of the gut microbiome in children in whom anti-islet cell autoimmunity developed. We investigated the microbiome of 298 stool samples prospectively taken up to age 3 years from 22 case children in whom anti-islet cell autoantibodies developed, and 22 matched control children who remained islet cell autoantibody-negative in follow-up. The microbiome changed markedly during the first year of life, and was further affected by breast-feeding, food introduction, and birth delivery mode. No differences between anti-islet cell autoantibody-positive and -negative children were found in bacterial diversity, microbial composition, or single-genus abundances. However, substantial alterations in microbial interaction networks were observed at age 0.5 and 2 years in the children in whom anti-islet cell autoantibodies developed. The findings underscore a role of the microbiome in the pathogenesis of anti-islet cell autoimmunity and type 1 diabetes.

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  • Authors+Show Affiliations

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    Scientific Computing Research Unit, Helmholtz Zentrum München, GermanyInstitute of Diabetes Research, Helmholtz Zentrum München, and Forschergruppe Diabetes, Klinikum rechts der Isar, Technische Universität München, Germany.

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    Scientific Computing Research Unit, Helmholtz Zentrum München, Germany.

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    Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL.

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    Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL.

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    Institute of Diabetes Research, Helmholtz Zentrum München, and Forschergruppe Diabetes, Klinikum rechts der Isar, Technische Universität München, Germany.

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    Scientific Computing Research Unit, Helmholtz Zentrum München, Germany.

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    Institute of Diabetes Research, Helmholtz Zentrum München, and Forschergruppe Diabetes, Klinikum rechts der Isar, Technische Universität München, Germany.

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    Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL.

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    Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL.

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    Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL.

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    Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL.

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    Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL.

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    Department of Pediatrics, University of Florida, Gainesville, FL.

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    Department of Pediatrics, University of Florida, Gainesville, FL.

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    Center for Regenerative Therapies, Dresden, and Paul Langerhans Institute Dresden, Technische Universität Dresden, GermanyInstitute for Diabetes and Obesity, Helmholtz Zentrum München, Germany.

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    Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, FL.

    Institute of Diabetes Research, Helmholtz Zentrum München, and Forschergruppe Diabetes, Klinikum rechts der Isar, Technische Universität München, Germany anette-g.ziegler@helmholtz-muenchen.de.

    Source

    Diabetes 63:6 2014 Jun pg 2006-14

    MeSH

    Autoimmunity
    Breast Feeding
    Case-Control Studies
    Child, Preschool
    Delivery, Obstetric
    Diabetes Mellitus, Type 1
    Environmental Exposure
    Feces
    Female
    Follow-Up Studies
    Gastrointestinal Tract
    Humans
    Infant
    Infant Food
    Infant Nutritional Physiological Phenomena
    Islets of Langerhans
    Male
    Microbiota
    Milk, Human
    Risk Factors

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    24608442

    Citation

    Endesfelder, David, et al. "Compromised Gut Microbiota Networks in Children With Anti-islet Cell Autoimmunity." Diabetes, vol. 63, no. 6, 2014, pp. 2006-14.
    Endesfelder D, zu Castell W, Ardissone A, et al. Compromised gut microbiota networks in children with anti-islet cell autoimmunity. Diabetes. 2014;63(6):2006-14.
    Endesfelder, D., zu Castell, W., Ardissone, A., Davis-Richardson, A. G., Achenbach, P., Hagen, M., ... Ziegler, A. G. (2014). Compromised gut microbiota networks in children with anti-islet cell autoimmunity. Diabetes, 63(6), pp. 2006-14. doi:10.2337/db13-1676.
    Endesfelder D, et al. Compromised Gut Microbiota Networks in Children With Anti-islet Cell Autoimmunity. Diabetes. 2014;63(6):2006-14. PubMed PMID: 24608442.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Compromised gut microbiota networks in children with anti-islet cell autoimmunity. AU - Endesfelder,David, AU - zu Castell,Wolfgang, AU - Ardissone,Alexandria, AU - Davis-Richardson,Austin G, AU - Achenbach,Peter, AU - Hagen,Michael, AU - Pflueger,Maren, AU - Gano,Kelsey A, AU - Fagen,Jennie R, AU - Drew,Jennifer C, AU - Brown,Christopher T, AU - Kolaczkowski,Bryan, AU - Atkinson,Mark, AU - Schatz,Desmond, AU - Bonifacio,Ezio, AU - Triplett,Eric W, AU - Ziegler,Anette-G, Y1 - 2014/03/07/ PY - 2014/3/11/entrez PY - 2014/3/13/pubmed PY - 2014/9/17/medline SP - 2006 EP - 14 JF - Diabetes JO - Diabetes VL - 63 IS - 6 N2 - The gut microbiome is suggested to play a role in the pathogenesis of autoimmune disorders such as type 1 diabetes. Evidence of anti-islet cell autoimmunity in type 1 diabetes appears in the first years of life; however, little is known regarding the establishment of the gut microbiome in early infancy. Here, we sought to determine whether differences were present in early composition of the gut microbiome in children in whom anti-islet cell autoimmunity developed. We investigated the microbiome of 298 stool samples prospectively taken up to age 3 years from 22 case children in whom anti-islet cell autoantibodies developed, and 22 matched control children who remained islet cell autoantibody-negative in follow-up. The microbiome changed markedly during the first year of life, and was further affected by breast-feeding, food introduction, and birth delivery mode. No differences between anti-islet cell autoantibody-positive and -negative children were found in bacterial diversity, microbial composition, or single-genus abundances. However, substantial alterations in microbial interaction networks were observed at age 0.5 and 2 years in the children in whom anti-islet cell autoantibodies developed. The findings underscore a role of the microbiome in the pathogenesis of anti-islet cell autoimmunity and type 1 diabetes. SN - 1939-327X UR - https://www.unboundmedicine.com/medline/citation/24608442/Compromised_gut_microbiota_networks_in_children_with_anti_islet_cell_autoimmunity_ L2 - http://diabetes.diabetesjournals.org/cgi/pmidlookup?view=long&pmid=24608442 DB - PRIME DP - Unbound Medicine ER -