Evidence map›Paper›PMID 26401004›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Maternal Antibiotic Treatment Protects Offspring from Diabetes Development in Nonobese Diabetic Mice by Generation of Tolerogenic APCs.

Youjia Hu, Jian Peng, Ningwen Tai, Changyun Hu, Xiaojun Zhang, F Susan Wong, Li Wen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
8.4field-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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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  13. mBio · 2021
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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

7 authors at 2 institutions in 3 countries.

Youjia HuSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; and.
Jian PengSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; and.
Ningwen TaiSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; and.
Changyun HuSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; and.
Xiaojun ZhangSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; and.
F Susan WongInstitute of Molecular and Experimental Medicine, Cardiff University School of Medicine, Cardiff CF14 4XN, United Kingdom.ORCID http://orcid.org/0000-0002-2812-8845
Li WenSection of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; and li.wen@yale.edu.
Yale University · USUniversity of Wales Institute Cardiff · SG

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
Dendritic cells in immuno-metabolic disorder in mouse and manR01DK100500 · NIDDK · YALE UNIVERSITY · PI WEN, LI · 2014 to 2017
$1.4M
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 P30-DK-45735NIDDK NIH HHS R01 DK088181NIDDK NIH HHS R01-DK-088181NIDDK NIH HHS R01 DK092882NIDDK NIH HHS R01-DK-092882NIDDK NIH HHS R01 DK100500NIDDK NIH HHS RC1 DK087699NIDDK NIH HHS RC1-DK-087699
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is a T cell-mediated autoimmune disease that involves the slow, progressive destruction of islet β cells and loss of insulin production, as a result of interaction with environmental factors, in genetically susceptible individuals. The gut microbiome is established very early in life. Commensal microbiota establish mutualism with the host and form an important part of the environment to which individuals are exposed in the gut, providing nutrients and shaping immune responses. In this study, we studied the impact of targeting most Gram-negative bacteria in the gut of NOD mice at different time points in their life, using a combination of three antibiotics--neomycin, polymyxin B, and streptomycin--on diabetes development. We found that the prenatal period is a critical time for shaping the immune tolerance in the progeny, influencing development of autoimmune diabetes. Prenatal neomycin, polymyxin B, and streptomycin treatment protected NOD mice from diabetes development through alterations in the gut microbiota, as well as induction of tolerogenic APCs, which led to reduced activation of diabetogenic CD8 T cells. Most importantly, we found that the protective effect was age dependent, and the most profound protection was found when the mice were treated before birth. This indicates the importance of the prenatal environment and early exposure to commensal bacteria in shaping the host immune system and health.

Indexed as

Immune ToleranceAge FactorsAnimalsAnti-Bacterial AgentsAntigen-Presenting CellsDiabetes Mellitus, Type 1FemaleIntestinesMiceMice, Inbred NODMicrobiotaNeomycinPolymyxin BPregnancyStreptomycinT-LymphocytesAnti-Bacterial AgentsNeomycinPolymyxin BStreptomycin

Identifiers

PMID26401004
PMCPMC4765177
OpenAlexW2293544761

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.