Evidence map›Paper›PMID 31281822›Full record

ReviewFrontiers in cardiovascular medicine2019

Platelet-Neutrophil Interplay: Insights Into Neutrophil Extracellular Trap (NET)-Driven Coagulation in Infection.

Amanda Z Zucoloto, Craig N Jenne

Abstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 2 pooled it
–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

127 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Exercise intensity and training alter the innate immune cell type and chromosomal origins of circulating cell-free DNA in humans.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Trial
  4. Trial
  5. Review
  6. Article
  7. A nomogram for assessing the risk of deep vein thrombosis following surgery for pilon fractures.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Endotheliopathy within the thromboinflammatory network of sepsis-induced coagulopathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

67 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

2 authors.

Amanda Z ZucolotoDepartment of Microbiology, Immunology and Infectious Diseases, Snyder Institute for Chronic Diseases, The University of Calgary, Calgary, AB, Canada.
Craig N JenneDepartment of Microbiology, Immunology and Infectious Diseases, Snyder Institute for Chronic Diseases, The University of Calgary, Calgary, AB, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Well established for their central role in hemostasis, platelets have increasingly been appreciated as immune cells in recent years. This emerging role should not come as a surprise as the central immune cells of invertebrates, hemocytes, are able to phagocytose, secrete soluble mediators and promote coagulation of hemolymph, blurring the line between immunity and hemostasis. The undeniable evolutionary link between coagulation and immunity becomes even clearer as the role of platelets in inflammation is better understood. Platelets exert a range of immune-related functions, many of which involve an intimate interplay with leukocytes. Platelets promote leukocyte recruitment via endothelial activation and can serve as "landing pads" for leukocytes, facilitating cellular adhesion in vascular beds devoid of classic adhesion molecules. Moreover, platelets enhance leukocyte function both through direct interactions and through release of soluble mediators. Among neutrophil-platelets interactions, the modulation of neutrophil extracellular traps (NETs) is of great interest. Platelets have been shown to induce NET formation; and, in turn, NET components further regulate platelet and neutrophil function. While NETs have been shown to ensnare and kill pathogens, they also initiate coagulation via thrombin activation. In fact, increased NET formation has been associated with hypercoagulability in septic patients as well as in chronic vascular disorders. This review will delve into current knowledge of platelet-neutrophil interactions, with a focus on NET-driven coagulation, in the context of infectious diseases. A better understanding of these mechanisms will shed a light on the therapeutic potential of uncoupling immunity and coagulation through targeting of NETs.

Indexed as

coagulationinflammationNETsneutrophil extracellular trapsneutrophilsplatelets

Identifiers

PMID31281822
PMCPMC6595231

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.