Evidence map›Paper›PMID 34456905›Full record

ArticleFrontiers in immunology2021

Mac-1 Receptor Clustering Initiates Production of Pro-Inflammatory, Antibacterial Extracellular Vesicles From Neutrophils.

Viktória Szeifert, Ferenc Kolonics, Balázs Bartos, Delaram Khamari, Pál Vági, László Barna, Erzsébet Ligeti, Ákos M Lőrincz

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The human factor H protein family - an update.Frontiers in immunology · 2024
    Review
  5. Targeting Neutrophil βBiomolecules · 2023
    Review
  6. Review
  7. 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

8 authors at 2 institutions in 1 country.

Viktória SzeifertDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Ferenc KolonicsDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Balázs BartosDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Delaram KhamariDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary.
Pál VágiNikon Center of Excellence, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
László BarnaNikon Center of Excellence, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
Erzsébet LigetiDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Ákos M LőrinczDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUHungarian Academy of Sciences · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depending on the prevailing environmental conditions, neutrophilic granulocytes release extracellular vesicles (EV) which have either anti-inflammatory effects on other neutrophils or pro-inflammatory and antibacterial effects. In the present study we investigated the molecular mechanisms underlying the biogenesis of functionally heterogenic EVs. We show that selective stimulation of Mac-1 integrin (complement receptor 3) by specific ligands initiates the generation of EVs which are able to impair bacterial growth and to induce the secretion of the pro-inflammatory cytokine IL-8 (aEV). However, direct Mac-1 stimulation results in aEV release only if neutrophils were activated on ligand coated surfaces whereas soluble ligands are ineffective. Using total internal reflection fluorescence (TIRF) microcopy, an increased clustering of Mac-1 molecules could be visualized in neutrophils added to C3bi coated surfaces; moreover antibody induced cluster formation triggers aEV release as well. Mac-1 induced production of aEV apparently necessitates a strong calcium signal as it fully depends on the presence of extracellular calcium. However, initiation of a strong calcium signal by an ionophore only results the generation of EV devoid of any antibacterial or pro-inflammatory effect. Our results thus demonstrate that stimulation and clustering of Mac-1 is necessary and sufficient for initiation of aEV biogenesis. In contrast, an intracellular calcium signal is necessary but by itself not sufficient for the production of antibacterial and pro-inflammatory EVs.

Indexed as

Cells, CulturedExtracellular VesiclesHumansMacrophage-1 AntigenNeutrophilsMacrophage-1 Antigencalcium signalextracellular vesiclesintegrinsMac-1neutrophilspro-inflammatory cytokinereceptor clustering

Identifiers

PMID34456905
PMCPMC8397541
OpenAlexW3189311175

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.