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Endesfelder, D. ; zu Castell, W. ; Ardissone, A.* ; Davis-Richardson, A.G.* ; Achenbach, P. ; Hagen, M. ; Pflueger, M. ; Gano, K.A.* ; Fagen, J.R.* ; Drew, J.C.* ; Brown, C.T.* ; Kolaczkowski, B.* ; Atkinson, M.J. ; Schatz, D.* ; Bonifacio, E. ; Triplett, E.W.* ; Ziegler, A.-G.

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

Diabetes 63, 2006-2014 (2014)
Verlagsversion DOI PMC
Closed
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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 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 who developed anti-islet cell autoimmunity. We investigated the microbiome of 298 stool samples prospectively taken up to age 3 years from 22 case children who developed anti-islet cell autoantibodies, and 22 matched control children who remained islet 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 who developed anti-islet cell autoantibodies. The findings underscore a role of the microbiome in the pathogenesis of anti-islet cell autoimmunity and type 1 diabetes.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Intestinal Microbiota; Lactobacillus-casei; Immune-system; Type-1; Model; Risk; Identification; Diversity; Differs; Ecology
Sprache englisch
Veröffentlichungsjahr 2014
HGF-Berichtsjahr 2014
ISSN (print) / ISBN 0012-1797
e-ISSN 1939-327X
Zeitschrift Diabetes
Quellenangaben Band: 63, Heft: 6, Seiten: 2006-2014 Artikelnummer: , Supplement: ,
Verlag American Diabetes Association
Verlagsort Alexandria, VA.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research (IDF)
Institute of Computational Biology (ICB)
Institute of Diabetes and Obesity (IDO)
Institute of Radiation Biology (ISB)
Institute of Pancreatic Islet Research (IPI)
German Center for Diabetes Reseach (DZD)
POF Topic(s) 30201 - Metabolic Health
30505 - New Technologies for Biomedical Discoveries
30502 - Diabetes: Pathophysiology, Prevention and Therapy
30202 - Environmental Health
Forschungsfeld(er) Helmholtz Diabetes Center
Enabling and Novel Technologies
Radiation Sciences
PSP-Element(e) G-502100-001
G-503890-001
G-502290-001
G-500200-001
PubMed ID 24608442
DOI 10.2337/db13-1676
WOS ID WOS:000336643900026
Scopus ID 84901330157
Erfassungsdatum 2014-03-12
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