Evidence map›Paper›PMID 31206609›Full record

ArticleBritish journal of pharmacology2019

Neutrophil extracellular trap-microparticle complexes trigger neutrophil recruitment via high-mobility group protein 1 (HMGB1)-toll-like receptors(TLR2)/TLR4 signalling.

Yongzhi Wang, Feifei Du, Avin Hawez, Matthias Mörgelin, Henrik Thorlacius

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Endothelial mechanobiology in atherosclerosis.Cardiovascular research · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Nets, pulmonary arterial hypertension, and thrombo-inflammation.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  18. The Role of HMGB1 in Rheumatic Diseases.Frontiers in immunology · 2022
    Review
  19. Correlation of HMGB1, PON-1, MCP-1, and PeriodontalJournal of healthcare engineering · 2022
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Yongzhi WangDepartment of Clinical Sciences, Section of Surgery, Lund University, Malmö, Sweden.
Feifei DuDepartment of Clinical Sciences, Section of Surgery, Lund University, Malmö, Sweden.
Avin HawezDepartment of Clinical Sciences, Section of Surgery, Lund University, Malmö, Sweden.
Matthias MörgelinColzyx AB, Lund, Sweden.
Henrik ThorlaciusDepartment of Clinical Sciences, Section of Surgery, Lund University, Malmö, Sweden.ORCID 0000-0001-7827-996X
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeRecent data suggest that neutrophil extracellular traps (NETs) form aggregates with microparticles (MPs) upon activation of neutrophils although the functional role of NET-MP complexes remain elusive. The objective of this study was to examine the role of NET-MP aggregates in leukocyte recruitment in vivo. EXPERIMENTAL APPROACH: PMA stimulation of murine bone marrow neutrophils generated NET-MP complexes and pretreatment with caspase and calpain inhibitors resulted in the formation of NETs depleted of MPs. Leukocyte-endothelium interactions were studied by using intravital microscopy of the mouse cremaster microcirculation. KEY

resultsIntrascrotal injection of NET-MP aggregates dose-dependently increased leukocyte recruitment. In contrast, leukocyte responses were markedly reduced after administration of NETs depleted of MPs. Neutrophil depletion abolished intravascular and extravascular leukocytes in response to challenge with NET-MP complexes. Electron microscopy revealed that NET-associated MPs express HMGB1. Notably, immunoneutralization of HMGB1 markedly decreased NET-MP complex-induced neutrophil accumulation. Moreover, inhibition of TLR2 and TLR4 significantly reduced neutrophil recruitment in response to NET-MP aggregates. CONCLUSIONS AND IMPLICATIONS: These data show that NET-MP complexes are potent inducers of neutrophil recruitment, which is dependent on HMGB1 expressed on MPs and mediated via TLR2 and TLR4. Blocking MP binding to NETs or downstream inhibition of the HMGB1-TLR2/TLR4 axis might provide useful targets to attenuating NET-dependent tissue damage in acute inflammation.

Indexed as

Signal TransductionAnimalsEndothelial CellsExtracellular TrapsHMGB1 ProteinMaleMiceMice, Inbred C57BLNeutrophilsToll-Like Receptor 2Toll-Like Receptor 4HMGB1 ProteinHMGB1 protein, mouseTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID31206609
PMCPMC6692579
OpenAlexW2953026859

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.