Evidence map›Paper›PMID 24767831›Full record

ArticleJournal of autoimmunity2014

Long term effect of gut microbiota transfer on diabetes development.

Jian Peng, Sukanya Narasimhan, Julian R Marchesi, Andrew Benson, F Susan Wong, Li Wen

Open access · greenAbstract read
In one paragraph

Article in Journal of autoimmunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
7.7field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

95 citing papers in PubMed, 150 citations in OpenAlex.

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  9. Reduced Expression of mInternational journal of molecular sciences · 2025
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  18. Periodontal bacteria influence systemic diseases through the gut microbiota.Frontiers in cellular and infection microbiology · 2024
    Review
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  20. Article

35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Jian PengSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Sukanya NarasimhanSection of Infectious Disease, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Julian R MarchesiCardiff School of Biosciences, Main Building, Museum Avenue, Cardiff University, Cardiff, UK; Centre for Digestive and Gut Health, Imperial College London, London, UK.
Andrew BensonDepartment of Food Science and Technology, University of Nebraska, Lincoln, NE, USA.
F Susan WongInstitute of Molecular and Experimental Medicine, School of Medicine, Cardiff University, Cardiff, UK.
Li WenSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address: li.wen@yale.edu.
Yale University · USCardiff University · GBUniversity of Nebraska–Lincoln · US

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Role of TLR9 in Beta Cell Function and DiabetesR01DK092882 · NIDDK · YALE UNIVERSITY · PI WEN, LI · 2012 to 2016
$1.8M
Environment, innate immunity and type 1 diabetesR01DK088181 · NIDDK · YALE UNIVERSITY · PI WEN, LI · 2010 to 2013
$1.4M
Effect of diet & commensal bacteria on diabetes outcome in NOD mouseRC1DK087699 · NIDDK · YALE UNIVERSITY · PI WEN, LI · 2009 to 2010
$991k
NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK088181NIDDK NIH HHS R01 DK092882NIDDK NIH HHS RC1 DK087699NIDDK NIH HHS RC1DK087699
6 · The paper itself

Abstract

The composition of the gut microbiome represents a very important environmental factor that influences the development of type 1 diabetes (T1D). We have previously shown that MyD88-deficient non-obese diabetic (MyD88-/-NOD) mice, that were protected from T1D development, had a different composition of gut microbiota compared to wild type NOD mice. The aim of our study was to investigate whether this protection could be transferred. We demonstrate that transfer of gut microbiota from diabetes-protected MyD88-deficient NOD mice, reduced insulitis and significantly delayed the onset of diabetes. Gut bacteria from MyD88-deficient mice, administered over a 3-week period, starting at 4 weeks of age, stably altered the family composition of the gut microbiome, with principally Lachnospiraceae and Clostridiaceae increased and Lactobacillaceae decreased. The transferred mice had a higher concentration of IgA and TGFβ in the lumen that was accompanied by an increase in CD8(+)CD103(+) and CD8αβ T cells in the lamina propria of the large intestine. These data indicate not only that gut bacterial composition can be altered after the neonatal/weaning period, but that the composition of the microbiome affects the mucosal immune system and can delay the development of autoimmune diabetes. This result has important implications for the development of probiotic treatment for T1D.

Indexed as

Diabetes Mellitus, ExperimentalIntestinesAnimalsBacteriaMiceMice, Inbred NODMice, KnockoutMicrobiotaMyeloid Differentiation Factor 88ProbioticsMyd88 protein, mouseMyeloid Differentiation Factor 88Gut microbiotaInnate immunityMucosal immunologyType 1 diabetes

Identifiers

PMID24767831
PMCPMC4361177
OpenAlexW2052152612

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.