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Imbalance of bacteriome profiles within the Finnish Diabetes Prediction and Prevention study: Parallel use of 16S profiling and virome sequencing in stool samples from children with islet autoimmunity and matched controls

O. Cinek, L. Kramna, J. Lin, S. Oikarinen, K. Kolarova, J. Ilonen, O. Simell, R. Veijola, R. Autio, H. Hyöty,

. 2017 ; 18 (7) : 588-598. [pub] 20161117

Jazyk angličtina Země Dánsko

Typ dokumentu časopisecké články, multicentrická studie

Perzistentní odkaz   https://www.medvik.cz/link/bmc18025253

Grantová podpora
NV15-29078A MZ0 CEP - Centrální evidence projektů

BACKGROUND: We set out to explore associations between the stool bacteriome profiles and early-onset islet autoimmunity, taking into account the interactions with the virus component of the microbiome. METHODS: Serial stool samples were longitudinally collected from 18 infants and toddlers with early-onset islet autoimmunity (median age 17.4 months) followed by type 1 diabetes, and 18 tightly matched controls from the Finnish Diabetes Prediction and Prevention (DIPP) cohort. Three stool samples were analyzed, taken 3, 6, and 9 months before the first detection of serum autoantibodies in the case child. The risk of islet autoimmunity was evaluated in relation to the composition of the bacteriome 16S rDNA profiles assessed by mass sequencing, and to the composition of DNA and RNA viromes. RESULTS: Four operational taxonomic units were significantly less abundant in children who later on developed islet autoimmunity as compared to controls-most markedly the species of Bacteroides vulgatus and Bifidobacterium bifidum. The alpha or beta diversity, or the taxonomic levels of bacterial phyla, classes or genera, showed no differences between cases and controls. A correlation analysis suggested a possible relation between CrAssphage signals and quantities of Bacteroides dorei. No apparent associations were seen between development of islet autoimmunity and sequences of yet unknown origin. CONCLUSIONS: The results confirm previous findings that an imbalance within the prevalent Bacteroides genus is associated with islet autoimmunity. The detected quantitative relation of the novel "orphan" bacteriophage CrAssphage with a prevalent species of the Bacteroides genus may exemplify possible modifiers of the bacteriome.

Citace poskytuje Crossref.org

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$a BACKGROUND: We set out to explore associations between the stool bacteriome profiles and early-onset islet autoimmunity, taking into account the interactions with the virus component of the microbiome. METHODS: Serial stool samples were longitudinally collected from 18 infants and toddlers with early-onset islet autoimmunity (median age 17.4 months) followed by type 1 diabetes, and 18 tightly matched controls from the Finnish Diabetes Prediction and Prevention (DIPP) cohort. Three stool samples were analyzed, taken 3, 6, and 9 months before the first detection of serum autoantibodies in the case child. The risk of islet autoimmunity was evaluated in relation to the composition of the bacteriome 16S rDNA profiles assessed by mass sequencing, and to the composition of DNA and RNA viromes. RESULTS: Four operational taxonomic units were significantly less abundant in children who later on developed islet autoimmunity as compared to controls-most markedly the species of Bacteroides vulgatus and Bifidobacterium bifidum. The alpha or beta diversity, or the taxonomic levels of bacterial phyla, classes or genera, showed no differences between cases and controls. A correlation analysis suggested a possible relation between CrAssphage signals and quantities of Bacteroides dorei. No apparent associations were seen between development of islet autoimmunity and sequences of yet unknown origin. CONCLUSIONS: The results confirm previous findings that an imbalance within the prevalent Bacteroides genus is associated with islet autoimmunity. The detected quantitative relation of the novel "orphan" bacteriophage CrAssphage with a prevalent species of the Bacteroides genus may exemplify possible modifiers of the bacteriome.
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$a Kramna, Lenka $u Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic.
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$a Lin, Jake $u BioMediTech, Computational Biology, University of Tampere, Tampere, Finland.
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$a Oikarinen, Sami $u School of Medicine, Department of Virology, University of Tampere, Tampere, Finland.
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$a Kolarova, Katerina $u Department of Pediatrics, 2nd Faculty of Medicine, Charles University in Prague and University Hospital Motol, Prague, Czech Republic.
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$a Ilonen, Jorma $u Immunogenetics Laboratory, University of Turku and Turku University Hospital, Turku, Finland.
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$a Simell, Olli $u Department of Pediatrics and Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland. Department of Pediatrics and Adolescent Medicine, Turku University Hospital, Turku, Finland.
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$a Veijola, Riitta $u Department of Pediatrics, University of Oulu and Oulu University Hospital, Oulu, Finland.
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$a Autio, Reija $u School of Health Sciences, University of Tampere, Tampere, Finland.
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$a Hyöty, Heikki $u School of Medicine, Department of Virology, University of Tampere, Tampere, Finland. Fimlab Laboratories, Pirkanmaa Hospital District, Tampere, Finland.
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