Evidence map›Paper›PMID 33643293›Full record

ArticleFrontiers in immunology2020

Bacterial and Fungal Toll-Like Receptor Activation Elicits Type I IFN Responses in Mast Cells.

Lisa Kornstädt, Sandra Pierre, Andreas Weigert, Stefanie Ebersberger, Tim J Schäufele, Anja Kolbinger, Tobias Schmid, Jennifer Cohnen, Dominique Thomas, Nerea Ferreirós and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  10. Microorganisms · 2022
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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

13 authors at 4 institutions in 1 country.

Lisa KornstädtInstitute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.
Sandra PierreInstitute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.
Andreas WeigertFaculty of Medicine, Institute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany.
Stefanie EbersbergerInstitute of Molecular Biology gGmbH, Mainz, Germany.
Tim J SchäufeleInstitute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.
Anja KolbingerInstitute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.
Tobias SchmidFaculty of Medicine, Institute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany.
Jennifer CohnenInstitute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.
Dominique ThomasInstitute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.
Nerea FerreirósInstitute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.
Bernhard BrüneFaculty of Medicine, Institute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany.
Ingo EbersbergerDepartment for Applied Bioinformatics, Institute for Cell Biology and Neuroscience, Goethe-University Frankfurt, Frankfurt, Germany.
Klaus ScholichInstitute of Clinical Pharmacology, University Hospital Goethe-University Frankfurt, Frankfurt, Germany.
Goethe University Frankfurt · DEInstitute of Molecular Biology · DEMerck (Germany) · DESenckenberg Biodiversity and Climate Research Centre · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Next to their role in IgE-mediated allergic diseases and in promoting inflammation, mast cells also have antiinflammatory functions. They release pro- as well as antiinflammatory mediators, depending on the biological setting. Here we aimed to better understand the role of mast cells during the resolution phase of a local inflammation induced with the Toll-like receptor (TLR)-2 agonist zymosan. Multiple sequential immunohistology combined with a statistical neighborhood analysis showed that mast cells are located in a predominantly antiinflammatory microenvironment during resolution of inflammation and that mast cell-deficiency causes decreased efferocytosis in the resolution phase. Accordingly, FACS analysis showed decreased phagocytosis of zymosan and neutrophils by macrophages in mast cell-deficient mice. mRNA sequencing using zymosan-induced bone marrow-derived mast cells (BMMC) revealed a strong type I interferon (IFN) response, which is known to enhance phagocytosis by macrophages. Both, zymosan and lipopolysaccharides (LPS) induced IFN-β synthesis in BMMCs in similar amounts as in bone marrow derived macrophages. IFN-β was expressed by mast cells in paws from naïve mice and during zymosan-induced inflammation. As described for macrophages the release of type I IFNs from mast cells depended on TLR internalization and endosome acidification. In conclusion, mast cells are able to produce several mediators including IFN-β, which are alone or in combination with each other able to regulate the phagocytotic activity of macrophages during resolution of inflammation.

Indexed as

AnimalsCells, CulturedChymasesDiphtheria ToxinDisease Models, AnimalFemaleInflammationInterferon Type ILipopolysaccharidesMacrophagesMaleMast CellsMiceMice, Inbred C57BLMice, TransgenicNeutrophilsChymasesCma1 protein, mouseDiphtheria ToxinInterferon Type ILipopolysaccharidesToll-Like ReceptorsZymosanIFN-βinflammationmast cellsphagocytosisresolutiontoll-like receptor

Identifiers

PMID33643293
PMCPMC7907501
OpenAlexW3132257048

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.