Evidence map›Paper›PMID 27011353›Full record

ArticleeLife2016

Disruption of glycolytic flux is a signal for inflammasome signaling and pyroptotic cell death.

Laura E Sanman, Yu Qian, Nicholas A Eisele, Tessie M Ng, Wouter A van der Linden, Denise M Monack, Eranthie Weerapana, Matthew Bogyo

Abstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
–field-weighted citation impact
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

117 citing papers in PubMed.

  1. Review
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  13. NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025
    Review
  14. Review
  15. Review
  16. Journal of inflammation research · 2025
    Review
  17. Review
  18. Article
  19. Review
  20. Article

57 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

8 authors.

Laura E SanmanDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, United States.
Yu QianDepartment of Chemistry, Boston College, Chestnut Hill, United States.
Nicholas A EiseleDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, United States.
Tessie M NgDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, United States.
Wouter A van der LindenDepartment of Pathology, Stanford University School of Medicine, Stanford, United States.
Denise M MonackDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, United States.
Eranthie WeerapanaDepartment of Chemistry, Boston College, Chestnut Hill, United States.
Matthew BogyoDepartment of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, United States.ORCID http://orcid.org/0000-0003-3753-4412

Funding

Vaccines and Diagnostics TrialsU54AI065359 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARBOUR, ALAN G. · 2005 to 2013
$88.8M
The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI STANLEY, SARAH A · 2004 to 2025
$45.5M
Small Molecule Imaging of Protease ActivityR01EB005011 · NIBIB · STANFORD UNIVERSITY · PI BOGYO, MATTHEW · 2005 to 2013
$3.0M
Chemical probes for specific targeting of matrix metallo proteasesR01CA179253 · NCI · STANFORD UNIVERSITY · PI BOGYO, MATTHEW · 2014 to 2018
$1.8M
NCI NIH HHS R01 CA179253NIAID NIH HHS AI063302NIAID NIH HHS AI065359NIAID NIH HHS P01 AI063302NIAID NIH HHS U54 AI065359NIBIB NIH HHS R01 EB005011
6 · The paper itself

Abstract

When innate immune cells such as macrophages are challenged with environmental stresses or infection by pathogens, they trigger the rapid assembly of multi-protein complexes called inflammasomes that are responsible for initiating pro-inflammatory responses and a form of cell death termed pyroptosis. We describe here the identification of an intracellular trigger of NLRP3-mediated inflammatory signaling, IL-1β production and pyroptosis in primed murine bone marrow-derived macrophages that is mediated by the disruption of glycolytic flux. This signal results from a drop of NADH levels and induction of mitochondrial ROS production and can be rescued by addition of products that restore NADH production. This signal is also important for host-cell response to the intracellular pathogen Salmonella typhimurium, which can disrupt metabolism by uptake of host-cell glucose. These results reveal an important inflammatory signaling network used by immune cells to sense metabolic dysfunction or infection by intracellular pathogens.

Indexed as

GlycolysisPyroptosisSignal TransductionAnimalsCells, CulturedInflammasomesInterleukin-1betaMacrophagesMiceNADNLR Family, Pyrin Domain-Containing 3 ProteinSalmonella typhimuriumIL1B protein, mouseInflammasomesInterleukin-1betaNADNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseCaspase-1glycolysisimmunologyinfectious diseaseinflammasomemicrobiologymouseNLRP3pyroptosisSalmonella typhimurium

Identifiers

PMID27011353
PMCPMC4846378

What OpenQuestion holds

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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.