Evidence map›Paper›PMID 26647392›Full record

ArticleBlood2016

ICAM-1-expressing neutrophils exhibit enhanced effector functions in murine models of endotoxemia.

Abigail Woodfin, Martina Beyrau, Mathieu-Benoit Voisin, Bin Ma, James R Whiteford, Peter L Hordijk, Nancy Hogg, Sussan Nourshargh

Abstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
–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

86 citing papers in PubMed.

  1. Article
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  7. Albumin-Bound STING Agonist Reprograms HSPCs to Antitumor Neutrophils Enhancing CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Review
  9. Article
  10. Psoriasis-like disease prevents squamous skin tumor development by neutrophil-driven inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  11. Article
  12. Review
  13. Article
  14. Target neutrophil heterogeneity and plasticity in cancer.Journal of hematology & oncology · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

26 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.

Abigail WoodfinWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom;
Martina BeyrauWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom;
Mathieu-Benoit VoisinWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom;
Bin MaWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom;
James R WhitefordWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom;
Peter L HordijkSanquin Research and Landsteiner Laboratory, Swammerdam Institute for Life Sciences Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; and.
Nancy HoggLeukocyte Adhesion Laboratory, Cancer Research UK London Research Institute, London, United Kingdom.
Sussan NoursharghWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom;

Funding

British Heart Foundation FS/11/19/28761Versus Arthritis 19207Versus Arthritis 19913Wellcome Trust 098291/Z/12/ZWellcome Trust 101604/Z/13/Z
6 · The paper itself

Abstract

Intracellular adhesion molecule-1 (ICAM-1) is a transmembrane glycoprotein expressed on the cell surface of numerous cell types such as endothelial and epithelial cells, vascular smooth muscle cells, and certain leukocyte subsets. With respect to the latter, ICAM-1 has been detected on neutrophils in several clinical and experimental settings, but little is known about the regulation of expression or function of neutrophil ICAM-1. In this study, we report on the de novo induction of ICAM-1 on the cell surface of murine neutrophils by lipopolysaccharide (LPS), tumor necrosis factor, and zymosan particles in vitro. The induction of neutrophil ICAM-1 was associated with enhanced phagocytosis of zymosan particles and reactive oxygen species (ROS) generation. Conversely, neutrophils from ICAM-1-deficient mice were defective in these effector functions. Mechanistically, ICAM-1-mediated intracellular signaling appeared to support neutrophil ROS generation and phagocytosis. In vivo, LPS-induced inflammation in the mouse cremaster muscle and peritoneal cavity led to ICAM-1 expression on intravascular and locally transmigrated neutrophils. The use of chimeric mice deficient in ICAM-1 on myeloid cells demonstrated that neutrophil ICAM-1 was not required for local neutrophil transmigration, but supported optimal intravascular and extravascular phagocytosis of zymosan particles. Collectively, the present results shed light on regulation of expression and function of ICAM-1 on neutrophils and identify it as an additional regulator of neutrophil effector responses in host defense.

Indexed as

AnimalsDisease Models, AnimalEndotoxemiaGene Expression RegulationIntercellular Adhesion Molecule-1LipopolysaccharidesMiceMice, KnockoutNeutrophilsPhagocytosisReactive Oxygen SpeciesTransendothelial and Transepithelial MigrationIcam1 protein, mouseIntercellular Adhesion Molecule-1LipopolysaccharidesReactive Oxygen Species

Identifiers

PMID26647392
PMCPMC4863345

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.