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

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.

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch

Erschienen in
Eosinophil‐derived IL ‐4 is necessary to establish the inflammatory structure in innate inflammation ; day:21 ; month:12 ; year:2022 ; extent:21
EMBO molecular medicine / European Molecular Biology Organization ; (21.12.2022) (gesamt 21)

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

DOI
10.15252/emmm.202216796
URN
urn:nbn:de:101:1-2022122114303386899462
Rechteinformation
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
15.08.2025, 07:32 MESZ

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