Evidence map›Paper›PMID 22143786›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Sterile inflammation of endothelial cell-derived apoptotic bodies is mediated by interleukin-1α.

Yaël Berda-Haddad, Stéphane Robert, Paul Salers, Leila Zekraoui, Catherine Farnarier, Charles A Dinarello, Françoise Dignat-George, Gilles Kaplanski

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 1 pooled it
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

144 citing papers in PubMed, 1 synthesis or guideline pooled it, 224 citations in OpenAlex.

  1. Pooled it
  2. Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026
    Review
  3. Bon appétit, your phagocyte.Cell death discovery · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Mesenchymal stem cell-derived extracellular vesicles in periodontal bone repair.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

84 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 at 3 institutions in 2 countries.

Yaël Berda-HaddadUnité Mixte de Recherche 608, Aix-Marseille University, 13005 Marseille, France.
Stéphane Robert
Paul Salers
Leila Zekraoui
Catherine Farnarier
Charles A Dinarello
Françoise Dignat-George
Gilles Kaplanski
Aix-Marseille Université · FRAssistance Publique Hôpitaux de Marseille · FRUniversity of Colorado Denver · US

Funding

Yeast-based HTS Assay Technologies for ProteasesR01AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1985 to 2025
$8.5M
VitiligoR01AR045584 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SPRITZ, RICHARD ANDREW · 1999 to 2014
$6.2M
Pathogenesis of Fever in ManR56AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 2016 to 2016
$311k
PATHOGENESIS OF FEVER IN HUMANSR37AI015614 · NIAID · UNIVERSITY OF COLORADO DENVER · PI DINARELLO, CHARLES ANTHONY · 1988 to 1998
–
NIAID NIH HHS AI-15614NIAMS NIH HHS AR-45584
6 · The paper itself

Abstract

Sterile inflammation resulting from cell death is due to the release of cell contents normally inactive and sequestered within the cell; fragments of cell membranes from dying cells also contribute to sterile inflammation. Endothelial cells undergoing stress-induced apoptosis release membrane microparticles, which become vehicles for proinflammatory signals. Here, we show that stress-activated endothelial cells release two distinct populations of particles: One population consists of membrane microparticles (<1 μm, annexin V positive without DNA and no histones) and another larger (1-3 μm) apoptotic body-like particles containing nuclear fragments and histones, representing apoptotic bodies. Contrary to present concepts, endothelial microparticles do not contain IL-1α and do not induce neutrophilic chemokines in vitro. In contrast, the large apoptotic bodies contain the full-length IL-1α precursor and the processed mature form. In vitro, these apoptotic bodies induce monocyte chemotactic protein-1 and IL-8 chemokine secretion in an IL-1α-dependent but IL-1β-independent fashion. Injection of these apoptotic bodies into the peritoneal cavity of mice induces elevated serum neutrophil-inducing chemokines, which was prevented by cotreatment with the IL-1 receptor antagonist. Consistently, injection of these large apoptotic bodies into the peritoneal cavity induced a neutrophilic infiltration that was prevented by IL-1 blockade. Although apoptosis is ordinarily considered noninflammatory, these data demonstrate that nonphagocytosed endothelial apoptotic bodies are inflammatory, providing a vehicle for IL-1α and, therefore, constitute a unique mechanism for sterile inflammation.

Indexed as

AnimalsApoptosisAutoimmunityCell-Derived MicroparticlesChemokine CCL2Endothelial CellsHistonesHumansHuman Umbilical Vein Endothelial CellsInflammationInterleukin-1alphaInterleukin 1 Receptor Antagonist ProteinInterleukin-8Lupus Erythematosus, SystemicMaleMiceChemokine CCL2HistonesInterleukin-1alphaInterleukin 1 Receptor Antagonist ProteinInterleukin-8

Identifiers

PMID22143786
PMCPMC3251090
OpenAlexW2029320450

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.