Evidence map›Paper›PMID 24356959›Full record

ArticleThe Journal of biological chemistry2014

Defects in mitochondrial clearance predispose human monocytes to interleukin-1β hypersecretion.

Robert van der Burgh, Lotte Nijhuis, Kalliopi Pervolaraki, Ewoud B Compeer, Lieneke H Jongeneel, Marielle van Gijn, Paul J Coffer, Michael P Murphy, Pier G Mastroberardino, Joost Frenkel and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.3field-weighted citation impact, top 3% 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, 90 citations in OpenAlex.

  1. Trial
  2. Mitochondrial DNA Release in Innate Immune Signaling.Annual review of biochemistry · 2023
    Review
  3. Article
  4. Article
  5. Review
  6. Immune Intervention in Sepsis.Frontiers in pharmacology · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Veterinary sciences · 2020
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Inflammation, a significant player of Ataxia-Telangiectasia pathogenesis?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Review
  20. Neuronal Dysfunction Associated with Cholesterol Deregulation.International journal of molecular sciences · 2018
    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 4 institutions in 2 countries.

Robert van der BurghFrom the Department of Pediatric Immunology and Infectious Diseases, University Medical Center Utrecht, Wilhelmina Children's Hospital, 3584 EA Utrecht, The Netherlands.
Lotte Nijhuis
Kalliopi Pervolaraki
Ewoud B Compeer
Lieneke H Jongeneel
Marielle van Gijn
Paul J Coffer
Michael P Murphy
Pier G Mastroberardino
Joost Frenkel
Marianne Boes
University Medical Center Utrecht · NLWilhelmina Children's Hospital · NLErasmus MC · NLMRC Mitochondrial Biology Unit · GB

Funding

Medical Research Council MC_U105663142
6 · The paper itself

Abstract

Most hereditary periodic fever syndromes are mediated by deregulated IL-1β secretion. The generation of mature IL-1β requires two signals: one that induces synthesis of inflammasome components and substrates and a second that activates inflammasomes. The mechanisms that mediate autoinflammation in mevalonate kinase deficiency, a periodic fever disease characterized by a block in isoprenoid biosynthesis, are poorly understood. In studying the effects of isoprenoid shortage on IL-1 β generation, we identified a new inflammasome activation signal that originates from defects in autophagy. We find that hypersecretion of IL-1β and IL-18 requires reactive oxygen species and is associated with an oxidized redox status of monocytes but not lymphocytes. IL-1β hypersecretion by monocytes involves decreased mitochondrial stability, release of mitochondrial content into the cytosol and attenuated autophagosomal degradation. Defective autophagy, as established by ATG7 knockdown, results in prolonged cytosolic retention of damaged mitochondria and increased IL-1β secretion. Finally, activation of autophagy in healthy but not mevalonate kinase deficiency patient cells reduces IL-1β secretion. Together, these results indicate that defective autophagy can prime monocytes for mitochondria-mediated NLRP3 inflammasome activation, thereby contributing to hypersecretion of IL-1β in mevalonate kinase deficiency.

Indexed as

AdolescentAutophagyCell LineChildChild, PreschoolCytosolDisease SusceptibilityDNA, MitochondrialHumansInflammasomesInterleukin-1betaMembrane Potential, MitochondrialMevalonate Kinase DeficiencyMitochondriaModels, BiologicalMonocytesDNA, MitochondrialIL1B protein, humanInflammasomesInterleukin-1betaTerpenesAutoinflammatory DisorderAutophagyInterleukinMitochondrial DNAMonocytesPeriodic FeverRedox Regulation

Identifiers

PMID24356959
PMCPMC3931060
OpenAlexW2117515483

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.