Evidence map›Paper›PMID 29293587›Full record

ArticlePloS one2018

Modulation of the diet and gastrointestinal microbiota normalizes systemic inflammation and β-cell chemokine expression associated with autoimmune diabetes susceptibility.

Angela M Henschel, Susanne M Cabrera, Mary L Kaldunski, Shuang Jia, Rhonda Geoffrey, Mark F Roethle, Vy Lam, Yi-Guang Chen, Xujing Wang, Nita H Salzman and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Effects of Free or ImmobilizedMicroorganisms · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Gut microbes
    Article
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

11 authors at 2 institutions in 1 country.

Angela M HenschelThe Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Susanne M CabreraThe Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Mary L KaldunskiThe Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Shuang JiaThe Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Rhonda GeoffreyThe Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Mark F RoethleThe Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Vy LamThe Department of Pediatrics at the Medical College of Wisconsin, and The Children's Research Institute of Children's Hospital of Wisconsin, Milwaukee, Wisconsin, United States of America.
Yi-Guang ChenThe Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.
Xujing WangNational Institute of Diabetes and Digestive and Kidney Diseases, the National Institutes of Health, Bethesda, Maryland, United States of America.
Nita H SalzmanThe Department of Pediatrics at the Medical College of Wisconsin, and The Children's Research Institute of Children's Hospital of Wisconsin, Milwaukee, Wisconsin, United States of America.
Martin J HessnerThe Max McGee National Research Center for Juvenile Diabetes at the Medical College of Wisconsin, Milwaukee, Wisconsin, United States of America.ORCID 0000-0001-9941-0314
Children's Hospital of Wisconsin · USNational Institutes of Health · US

Funding

Mechanistic and Therapeutic Role of the CD137-CD137L Axis in Type 1 DiabetesR01DK107541 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG, RIDGWAY, WILLIAM M · 2016 to 2025
$5.6M
Dissection of cellular interactions in T1DM with integrated functional genomicsR01AI078713 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI HESSNER, MARTIN J · 2009 to 2013
$1.7M
Quantitative measurement of T1D risk through molecular signature analysisDP3DK098161 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI GREENBAUM, CARLA J, HESSNER, MARTIN J · 2013 to 2013
$857k
Plasma Induced Signatures as a Measure of Immunomodulation in T1D Clinical TrialsR56DK108802 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI HESSNER, MARTIN J · 2016 to 2017
$608k
NIAID NIH HHS R01 AI078713NIDDK NIH HHS DP3 DK098161NIDDK NIH HHS R01 DK107541NIDDK NIH HHS R56 DK108802
6 · The paper itself

Abstract

Environmental changes associated with modern lifestyles may underlie the rising incidence of Type 1 diabetes (T1D). Our previous studies of T1D families and the BioBreeding (BB) rat model have identified a peripheral inflammatory state that is associated with diabetes susceptibility, consistent with pattern recognition receptor ligation, but is independent of disease progression. Here, compared to control strains, islets of spontaneously diabetic BB DRlyp/lyp and diabetes inducible BB DR+/+ weanlings provided a standard cereal diet expressed a robust proinflammatory transcriptional program consistent with microbial antigen exposure that included numerous cytokines/chemokines. The dependence of this phenotype on diet and gastrointestinal microbiota was investigated by transitioning DR+/+ weanlings to a gluten-free hydrolyzed casein diet (HCD) or treating them with antibiotics to alter/reduce pattern recognition receptor ligand exposure. Bacterial 16S rRNA gene sequencing revealed that these treatments altered the ileal and cecal microbiota, increasing the Firmicutes:Bacteriodetes ratio and the relative abundances of lactobacilli and butyrate producing taxa. While these conditions did not normalize the inherent hyper-responsiveness of DR+/+ rat leukocytes to ex vivo TLR stimulation, they normalized plasma cytokine levels, plasma TLR4 activity levels, the proinflammatory islet transcriptome, and β-cell chemokine expression. In lymphopenic DRlyp/lyp rats, HCD reduced T1D incidence, and the introduction of gluten to this diet induced islet chemokine expression and abrogated protection from diabetes. Overall, these studies link BB rat islet-level immunocyte recruiting potential, as measured by β-cell chemokine expression, to a genetically controlled immune hyper-responsiveness and innate inflammatory state that can be modulated by diet and the intestinal microbiota.

Indexed as

DietGastrointestinal MicrobiomeAnimalsChemokinesCytokinesDiabetes Mellitus, Type 1Gene Expression ProfilingImmunity, InnateInflammationInflammation MediatorsIslets of LangerhansRatsRats, Inbred F344Transcription, GeneticChemokinesCytokinesInflammation Mediators

Identifiers

PMID29293587
PMCPMC5749787
OpenAlexW2781538922

What OpenQuestion holds

Textmetadata
LicenceCC0
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.