Human gut microbiota transferred to germ-free NOD mice modulate the progression towards type 1 diabetes regardless of the pace of beta cell function loss in the donor
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
31025045
DOI
10.1007/s00125-019-4869-2
PII: 10.1007/s00125-019-4869-2
Knihovny.cz E-zdroje
- Klíčová slova
- Germ-free NOD mice, Human gut microbiome transfer, Type 1 diabetes,
- MeSH
- diabetes mellitus 1. typu mikrobiologie terapie MeSH
- feces mikrobiologie MeSH
- lidé MeSH
- mikrobiota fyziologie MeSH
- modely nemocí na zvířatech MeSH
- myši inbrední NOD MeSH
- myši MeSH
- progrese nemoci MeSH
- střevní mikroflóra fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
AIMS/HYPOTHESIS: This study aimed to assess the ability of human gut microbiota to delay the onset of type 1 diabetes when transferred into germ-free NOD mice. METHODS: Two children with rapid and three children with slow beta cell function loss (as assessed by C-peptide AUC change in the mixed-meal tolerance tests performed 1 and 12 months after type 1 diabetes onset), participating in an ongoing trial with gluten-free diet, donated faeces, which were transferred into germ-free NOD mice. The mice were subsequently followed for diabetes incidence. RESULTS: The bacterial profiles of bacteriome-humanised mice had significantly (p < 10-5) lower alpha diversity than the donor material, with marked shifts in ratios between the main phyla. Diabetes onset was significantly delayed in all bacteriome-humanised colonies vs germ-free NOD mice, but the pace of beta cell loss was not transferable to the mouse model. CONCLUSIONS/INTERPRETATION: Germ-free NOD mice colonised with human gut microbiome are able to adopt a large proportion of transferred bacterial content, although the ratios of main phyla are reproduced only suboptimally. The recipient mice did not replicate the phenotype of the stool donor in relation to the pace towards type 1 diabetes. TRIAL REGISTRATION: ClinicalTrials.gov NCT02867436.
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Diabetologia. 2010 Apr;53(4):741-8 PubMed
Mucosal Immunol. 2012 Sep;5(5):567-79 PubMed
Nature. 2013 Aug 8;500(7461):232-6 PubMed
Diabetes Res Clin Pract. 2013 May;100(2):203-9 PubMed
Science. 2011 Jan 21;331(6015):337-41 PubMed
Diabetologia. 2005 Aug;48(8):1565-75 PubMed
Curr Diab Rep. 2017 Sep 23;17(11):105 PubMed
Sci Transl Med. 2009 Nov 11;1(6):6ra14 PubMed
Diabetologia. 2014 Aug;57(8):1569-77 PubMed
ISME J. 2017 Mar;11(3):676-690 PubMed
Cell Mol Immunol. 2011 Mar;8(2):110-20 PubMed
Appl Environ Microbiol. 2013 Sep;79(17):5112-20 PubMed
Gut. 2018 Aug;67(8):1445-1453 PubMed
ILAR J. 2004;45(3):278-91 PubMed
Gut Microbes. 2012 May-Jun;3(3):234-49 PubMed
Am J Gastroenterol. 2012 May;107(5):761-7 PubMed
Diabetologia. 2011 Jun;54(6):1398-406 PubMed
Pediatr Diabetes. 2017 Nov;18(7):588-598 PubMed
Front Microbiol. 2014 Dec 10;5:678 PubMed
ClinicalTrials.gov
NCT02867436
