Evidence map›Paper›PMID 26102221›Full record

ArticleNature communications2015

Evidence that asthma is a developmental origin disease influenced by maternal diet and bacterial metabolites.

Alison N Thorburn, Craig I McKenzie, Sj Shen, Dragana Stanley, Laurence Macia, Linda J Mason, Laura K Roberts, Connie H Y Wong, Raymond Shim, Remy Robert and 12 more

Open access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 492 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
492citing papers in PubMed, 5 pooled it
38.1field-weighted citation impact, top 1% 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

492 citing papers in PubMed, 5 syntheses or guidelines pooled it, 890 citations in OpenAlex.

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432 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

22 authors at 8 institutions in 3 countries.

Alison N ThorburnDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Craig I McKenzieDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Sj ShenDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.ORCID 0000000210041936
Dragana StanleySchool of Medical and Applied Sciences, Central Queensland University, Rockhampton, Queensland 4702, Australia.
Laurence MaciaDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Linda J MasonDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Laura K RobertsDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Connie H Y WongDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Raymond ShimDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Remy RobertDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Nina Chevalier1] Department of Immunology, Monash University, Clayton, Victoria 3800, Australia [2] Department of Rheumatology and Clinical Immunology, University Medical Center, 79106 Freiburg, Germany.
Jian K TanDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Eliana MariñoDepartment of Immunology, Monash University, Clayton, Victoria 3800, Australia.
Rob J Moore1] CSIRO Animal, Food, and Health Sciences, Geelong, Victoria 3220, Australia [2] Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia.
Lee WongDepartment of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia.
Malcolm J McConville1] Department of Biochemistry and Molecular Biology, Bio21 Institute of Molecular Science and Biotechnology, University of Melbourne, Melbourne, Victoria 3010, Australia [2] Metabolomics Australia, Bio21 Institute of Molecular Sciences and Biotechnology, University of Melbourne, Melbourne, Victoria 3010, Australia.
Dedreia L TullMetabolomics Australia, Bio21 Institute of Molecular Sciences and Biotechnology, University of Melbourne, Melbourne, Victoria 3010, Australia.
Lisa G WoodCentre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales 2300, Australia.
Vanessa E MurphyCentre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales 2300, Australia.
Joerg MattesCentre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales 2300, Australia.
Peter G GibsonCentre for Asthma and Respiratory Disease, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales 2300, Australia.
Charles R Mackay1] Department of Immunology, Monash University, Clayton, Victoria 3800, Australia [2] Charles Perkins Centre, Sydney University Medical School, University of Sydney, Sydney, New South Wales 2006, Australia.
Monash University · AUHunter Medical Research Institute · AUBiotechnology Institute · USCentral Queensland University · AUCommonwealth Scientific and Industrial Research Organisation · AUThe University of Melbourne · AUThe University of Sydney · AUUniversity Medical Center Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is prevalent in Western countries, and recent explanations have evoked the actions of the gut microbiota. Here we show that feeding mice a high-fibre diet yields a distinctive gut microbiota, which increases the levels of the short-chain fatty acid, acetate. High-fibre or acetate-feeding led to marked suppression of allergic airways disease (AAD, a model for human asthma), by enhancing T-regulatory cell numbers and function. Acetate increases acetylation at the Foxp3 promoter, likely through HDAC9 inhibition. Epigenetic effects of fibre/acetate in adult mice led us to examine the influence of maternal intake of fibre/acetate. High-fibre/acetate feeding of pregnant mice imparts on their adult offspring an inability to develop robust AAD. High fibre/acetate suppresses expression of certain genes in the mouse fetal lung linked to both human asthma and mouse AAD. Thus, diet acting on the gut microbiota profoundly influences airway responses, and may represent an approach to prevent asthma, including during pregnancy.

Indexed as

DietGastrointestinal MicrobiomeAcetatesAcetylationAnimalsAsthmaDietary FiberDisease Models, AnimalEpigenesis, GeneticFatty Acids, VolatileFemaleForkhead Transcription FactorsHistone DeacetylasesMicePregnancyPrenatal Exposure Delayed EffectsAcetatesDietary FiberFatty Acids, VolatileForkhead Transcription FactorsFoxp3 protein, mouseHdac9 protein, mouseHistone DeacetylasesRepressor Proteins

Identifiers

PMID26102221
OpenAlexW769303411

What OpenQuestion holds

Textmetadata
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.