Evidence map›Paper›PMID 25589762›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Inflammasome-induced IL-1β secretion in microglia is characterized by delayed kinetics and is only partially dependent on inflammatory caspases.

Saskia M Burm, Ella A Zuiderwijk-Sick, Anke E J 't Jong, Céline van der Putten, Jennifer Veth, Ivanela Kondova, Jeffrey J Bajramovic

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Inflammasome Molecular Insights in Autoimmune Diseases.Current issues in molecular biology · 2024
    Review
  5. Review
  6. Article
  7. Selective inhibition of PKR by C16 accelerates diabetic wound healing by inhibiting NALP3 expression in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Inflammasome Activation in Parkinson's Disease.Journal of Parkinson's disease · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Microglia in neurodegenerative diseases.Neural regeneration research · 2021
    Review
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 3 institutions in 4 countries.

Saskia M BurmAlternatives Unit.
Ella A Zuiderwijk-SickAlternatives Unit.
Anke E J 't JongAlternatives Unit.
Céline van der PuttenAlternatives Unit.
Jennifer VethAlternatives Unit.
Ivanela KondovaAnimal Science Department, Biomedical Primate Research Centre, 2288 GJ Rijswijk, The Netherlands.
Jeffrey J BajramovicAlternatives Unit, bajramovic@bprc.nl.ORCID http://orcid.org/0000-0002-6504-3437
University of Development Alternative · BDAltera (United States) · USBiomedical Primate Research Centre · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammasomes are multiprotein complexes that link pathogen recognition and cellular stress to the processing of the proinflammatory cytokine interleukin-1β (IL-1β). Whereas inflammasome-mediated activation is heavily studied in hematopoietic macrophages and dendritic cells, much less is known about microglia, resident tissue macrophages of the brain that originate from a distinct progenitor. To directly compare inflammasome-mediated activation in different types of macrophages, we isolated primary microglia and hematopoietic macrophages from adult, healthy rhesus macaques. We analyzed the expression profile of NOD (nucleotide-binding oligomerization domain)-like receptors, adaptor proteins, and caspases and characterized inflammasome activation and regulation in detail. We here demonstrate that primary microglia can respond to the same innate stimuli as hematopoietic macrophages. However, microglial responses are more persistent due to lack of negative regulation on pro-IL-1β expression. In addition, we show that while caspase 1, 4, and 5 activation is pivotal for inflammasome-induced IL-1β secretion by hematopoietic macrophages, microglial secretion of IL-1β is only partially dependent on these inflammatory caspases. These results identify key cell type-specific differences that may aid the development of strategies to modulate innate immune responses in the brain.

Indexed as

AnimalsCaspasesCells, CulturedFemaleInflammasomesInterleukin-1betaKineticsMacaca mulattaMacrophagesMaleMicrogliaNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinReaction TimeCaspasesInflammasomesInterleukin-1betaNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinIL-1βinflammasomeinflammatory caspasesmacrophagesmicroglia

Identifiers

PMID25589762
PMCPMC6605364
OpenAlexW2020008646

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.