Evidence map›Paper›PMID 26516283›Full record

ArticleScience (New York, N.Y.)2015

Disease tolerance mediated by microbiome E. coli involves inflammasome and IGF-1 signaling.

Alexandria M Palaferri Schieber, Yujung Michelle Lee, Max W Chang, Mathias Leblanc, Brett Collins, Michael Downes, Ronald M Evans, Janelle S Ayres

Abstract read
In one paragraph

Article in Science (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 1 pooled it
16.8field-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

105 citing papers in PubMed, 1 synthesis or guideline pooled it, 195 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Translational control of innate barrier defense by the gut microbiota.bioRxiv : the preprint server for biology · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Antioxidants (Basel, Switzerland) · 2025
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Alexandria M Palaferri SchieberNomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Yujung Michelle LeeNomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Max W ChangIntegrative Genomics and Bioinformatics Core, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Mathias LeblancGene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Brett CollinsGene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Michael DownesGene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Ronald M EvansGene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA. Howard Hughes Medical Institute, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Janelle S AyresNomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA. jayres@salk.edu.
Salk Institute for Biological Studies · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
HORMONAL REGULATION OF MAMMALIAN GENE EXPRESSIONR37DK057978 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2000 to 2019
$16.0M
Tolerance defenses in host-microbiota interactionsR01AI114929 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI AYRES, JANELLE S · 2015 to 2025
$4.9M
Howard Hughes Medical InstituteNCI NIH HHS CA014195NCI NIH HHS P30 CA014195NIAID NIH HHS R01 AI114929NIAID NIH HHS R01AI114929NIDDK NIH HHS DK0577978NIDDK NIH HHS R37 DK057978
6 · The paper itself

Abstract

Infections and inflammation can lead to cachexia and wasting of skeletal muscle and fat tissue by as yet poorly understood mechanisms. We observed that gut colonization of mice by a strain of Escherichia coli prevents wasting triggered by infections or physical damage to the intestine. During intestinal infection with the pathogen Salmonella Typhimurium or pneumonic infection with Burkholderia thailandensis, the presence of this E. coli did not alter changes in host metabolism, caloric uptake, or inflammation but instead sustained signaling of the insulin-like growth factor 1/phosphatidylinositol 3-kinase/AKT pathway in skeletal muscle, which is required for prevention of muscle wasting. This effect was dependent on engagement of the NLRC4 inflammasome. Therefore, this commensal promotes tolerance to diverse diseases.

Indexed as

MicrobiotaAnimalsApoptosis Regulatory ProteinsBiosynthetic PathwaysBurkholderiaBurkholderia InfectionsCalcium-Binding ProteinsEscherichia coliInflammasomesInsulin-Like Growth Factor IIntestinesMiceMice, Inbred C57BLMuscle, SkeletalPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktApoptosis Regulatory ProteinsCalcium-Binding ProteinsInflammasomesInsulin-Like Growth Factor IIpaf protein, mousePhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-akt

Identifiers

PMID26516283
PMCPMC4732872
OpenAlexW2285543512

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.