Evidence map›Paper›PMID 32191647›Full record

ArticleThe Journal of clinical investigation2020

Semaphorin 3F signaling actively retains neutrophils at sites of inflammation.

Tracie Plant, Suttida Eamsamarng, Manuel A Sanchez-Garcia, Leila Reyes, Stephen A Renshaw, Patricia Coelho, Ananda S Mirchandani, Jessie-May Morgan, Felix E Ellett, Tyler Morrison and 13 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026
    Review
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  11. Wound Healing Insights from Flies and Fish.Cold Spring Harbor perspectives in biology · 2022
    Review
  12. Article
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  14. Review
  15. Article
  16. Review
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

23 authors at 5 institutions in 3 countries.

Tracie PlantUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Suttida EamsamarngDepartment of Infection, Immunity and Cardiovascular Disease and.
Manuel A Sanchez-GarciaUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Leila ReyesUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Stephen A RenshawDepartment of Infection, Immunity and Cardiovascular Disease and.
Patricia CoelhoUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Ananda S MirchandaniUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Jessie-May MorganUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Felix E EllettDepartment of Infection, Immunity and Cardiovascular Disease and.
Tyler MorrisonUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Duncan HumphriesUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Emily R WattsUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Fiona MurphyUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Ximena L Raffo-IraolagoitiaCancer Research UK Beatson Institute, Glasgow, United Kingdom.
Ailiang ZhangUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Jenna L CashUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Catherine LoynesDepartment of Infection, Immunity and Cardiovascular Disease and.
Philip M ElksDepartment of Infection, Immunity and Cardiovascular Disease and.
Freek Van EedenDepartment of Infection, Immunity and Cardiovascular Disease and.
Leo M CarlinCancer Research UK Beatson Institute, Glasgow, United Kingdom.
Andrew Jw FurleyBateson Centre, University of Sheffield, Sheffield, United Kingdom.
Moira Kb WhyteUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Sarah R WalmsleyUniversity of Edinburgh Centre for Inflammation Research, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Centre for Inflammation Research · GBImmunité et Cancer · FRCancer Research UK Scotland Institute · GBMassachusetts General Hospital · USUniversity of Sheffield · GB

Funding

Cancer Research UK 23983Cancer Research UK A17196Cancer Research UK A23983Cancer Research UK C62207/A24495Medical Research Council G0700091Medical Research Council G0701932Medical Research Council MR/M004864/1Medical Research Council MR/N02995X/1Medical Research Council MR/P020941/1Wellcome Trust 098516Wellcome Trust 110086/Z/15/ZWellcome Trust 202581/Z/16/ZWellcome Trust 209220Wellcome Trust 209220/Z/17/ZWellcome Trust R43999
6 · The paper itself

Abstract

Neutrophilic inflammation is central to disease pathogenesis, for example, in chronic obstructive pulmonary disease, yet the mechanisms that retain neutrophils within tissues remain poorly understood. With emerging evidence that axon guidance factors can regulate myeloid recruitment and that neutrophils can regulate expression of a class 3 semaphorin, SEMA3F, we investigated the role of SEMA3F in inflammatory cell retention within inflamed tissues. We observed that neutrophils upregulate SEMA3F in response to proinflammatory mediators and following neutrophil recruitment to the inflamed lung. In both zebrafish tail injury and murine acute lung injury models of neutrophilic inflammation, overexpression of SEMA3F delayed inflammation resolution with slower neutrophil migratory speeds and retention of neutrophils within the tissues. Conversely, constitutive loss of sema3f accelerated egress of neutrophils from the tail injury site in fish, whereas neutrophil-specific deletion of Sema3f in mice resulted in more rapid neutrophil transit through the airways, and significantly reduced time to resolution of the neutrophilic response. Study of filamentous-actin (F-actin) subsequently showed that SEMA3F-mediated retention is associated with F-actin disassembly. In conclusion, SEMA3F signaling actively regulates neutrophil retention within the injured tissues with consequences for neutrophil clearance and inflammation resolution.

Indexed as

AnimalsCell MovementHumansInflammationMembrane ProteinsMiceNerve Tissue ProteinsNeutrophilsSignal TransductionUp-RegulationZebrafishZebrafish ProteinsMembrane ProteinsNerve Tissue ProteinsSEMA3F protein, humanSema3f protein, mouseZebrafish ProteinsCell migration/adhesionCellular immune responseInflammationNeutrophilsPulmonology

Identifiers

PMID32191647
PMCPMC7259996
OpenAlexW3011282952

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.