Evidence map›Paper›PMID 36541656›Full record

ArticleEMBO molecular medicine2023

Eosinophil-derived IL-4 is necessary to establish the inflammatory structure in innate inflammation.

Anja Kolbinger, Tim J Schäufele, Hanna Steigerwald, Joschua Friedel, Sandra Pierre, Gerd Geisslinger, Klaus Scholich

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. 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
1.8field-weighted citation impact, top 14% 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, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
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

7 authors at 1 institution in 1 country.

Anja KolbingerInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Frankfurt, Germany.ORCID 0000-0003-3120-7277
Tim J SchäufeleInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Frankfurt, Germany.
Hanna SteigerwaldInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Frankfurt, Germany.ORCID 0000-0002-4219-6270
Joschua FriedelInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Frankfurt, Germany.ORCID 0000-0002-0186-6565
Sandra PierreInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Frankfurt, Germany.
Gerd GeisslingerInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Frankfurt, Germany.
Klaus ScholichInstitute of Clinical Pharmacology, Goethe-University Frankfurt, Frankfurt, Germany.ORCID 0000-0003-3744-0854
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogen-induced inflammation comprises pro- and anti-inflammatory processes, which ensure pathogen removal and containment of the proinflammatory activities. Here, we aimed to identify the development of inflammatory microenvironments and their maintenance throughout the course of a toll-like receptor 2-mediated paw inflammation. Within 24 h after pathogen-injection, the immune cells were organized in three zones, which comprised a pathogen-containing "core-region", a bordering proinflammatory (PI)-region and an outer anti-inflammatory (AI)-region. Eosinophils were present in all three inflammatory regions and adapted their cytokine profile according to their localization. Eosinophil depletion reduced IL-4 levels and increased edema formation as well as mechanical and thermal hypersensitivities during resolution of inflammation. Also, in the absence of eosinophils PI- and AI-regions could not be determined anymore, neutrophil numbers increased, and efferocytosis as well as M2-macrophage polarization were reduced. IL-4 administration restored in eosinophil-depleted mice PI- and AI-regions, normalized neutrophil numbers, efferocytosis, M2-macrophage polarization as well as resolution of zymosan-induced hypersensitivity. In conclusion, IL-4-expressing eosinophils support the resolution of inflammation by enabling the development of an anti-inflammatory framework, which encloses proinflammatory regions.

Indexed as

EosinophilsInterleukin-4AnimalsAnti-Inflammatory AgentsInflammationMiceNeutrophilsAnti-Inflammatory AgentsIl4 protein, mouseInterleukin-4eosinophilinnate inflammationinterleukin-4macrophagesmicroenvironments

Identifiers

PMID36541656
PMCPMC9906331
OpenAlexW4312065442

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.