Evidence map›Paper›PMID 40692416›Full record

ArticleDisease models & mechanisms2025

A subset of neutrophil phagosomes is characterised by pulses of Class I PI3K activity.

Clare F Muir, Constantino Carlos Reyes-Aldasoro, Tomasz K Prajsnar, Bartosz J Michno, Justyna Cholewa-Waclaw, Yin X Ho, Audrey Bernut, Catherine A Loynes, Stone Elworthy, Kieran A Bowden and 6 more

Erratum issuedAbstract read
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In one paragraph

Article in Disease models & mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Clare F MuirBateson Centre, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2TN, UK.ORCID 0009-0002-6158-9392
Constantino Carlos Reyes-AldasoroDepartment of Computer Science, School of Science and Technology, City, University of London, London EC1V 0HB, UK.
Tomasz K PrajsnarDepartment of Evolutionary Immunology, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University, Kraków 30-387, Poland.
Bartosz J MichnoDepartment of Evolutionary Immunology, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University, Kraków 30-387, Poland.
Justyna Cholewa-WaclawCentre of Inflammation, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh EH16 4UU, UK.
Yin X HoBateson Centre, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2TN, UK.
Audrey BernutLaboratory of Pathogens and Host Immunity, Université de Montpellier, Montpellier 34090, France.
Catherine A LoynesBateson Centre, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2TN, UK.
Stone ElworthyBateson Centre, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2TN, UK.
Kieran A BowdenBateson Centre, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2TN, UK.
Ashley J CadbyDepartment of Physics and Astronomy, University of Sheffield, Sheffield S3 7RH, UK.
Lynne R PrinceBateson Centre, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2TN, UK.
Jason S KingSchool of Biosciences, University of Sheffield, Sheffield S10 2TN, UK.
Felix EllettCentre for Engineering in Medicine and Surgery, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Shriners Burns Hospital, Boston, MA 02114, USA.
Alison M CondliffeBateson Centre, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2TN, UK.
Stephen A RenshawBateson Centre, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2TN, UK.ORCID 0000-0003-1790-1641

Funding

Biotechnology and Biological Sciences Research Council B/V019368/1Narodowe Centrum Nauki UMO-2019/34/E/NZ6/00137University of SheffieldWellcome TrustWellcome Trust (R/151624Wellcome Trust R/151624
6 · The paper itself

Abstract

Class I PI3 kinases (PI3Ks) coordinate the delivery of microbicidal effectors to the phagosome by forming phosphatidylinositol (3,4,5)-trisphosphate (PIP3). However, the dynamics of PIP3 in neutrophils during a live bacterial tissue infection are unknown. We therefore developed an in vivo, live zebrafish infection model that enables visualisation of dynamic changes in Class 1 PI3K signalling in neutrophil phagosomes in real time. We identified that, on ∼12% of neutrophil phagosomes, PHAkt-eGFP, a reporter for Class 1 PI3K signalling, repeatedly fades and re-recruits in pulsatile bursts. This phenomenon occurred on phagosomes containing live and dead bacteria as well as beads, and was dependent on the activity of the Class 1 PI3K isoform PI3Kγ. Detailed imaging suggested that pulsing phagosomes represent neutrophils transiently re-opening and re-closing phagosomes, a conclusion supported by observations that a subset of phagosomes in human neutrophils rapidly accumulate dye from the extracellular space. Therefore, we propose that some neutrophil phagosomes remain unsealed and are consequently able to exchange contents with the extracellular environment, with implications for phagosome fate and communication with surrounding cells.

Indexed as

Class I Phosphatidylinositol 3-KinasesNeutrophilsPhagosomesAnimalsGreen Fluorescent ProteinsHumansPhagocytosisPhosphatidylinositol PhosphatesSignal TransductionZebrafishClass I Phosphatidylinositol 3-KinasesGreen Fluorescent ProteinsPhosphatidylinositol PhosphatesNeutrophilsPhagocytosisPhagosome maturationPhosphatidylinositol (3,4,5)-trisphosphateZebrafish

Identifiers

PMID40692416
PMCPMC12444860

What OpenQuestion holds

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Registered trials

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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.