The chemokine CCL1 facilitates pulmonary fibrosis by promoting macrophage migration and M2 polarization.
AMFR
CCR8
CREB/C/EBPβ signaling pathway
Chemokine CCL1
M2 polarization
Macrophage
Pulmonary fibrosis
Journal
International immunopharmacology
ISSN: 1878-1705
Titre abrégé: Int Immunopharmacol
Pays: Netherlands
ID NLM: 100965259
Informations de publication
Date de publication:
Jul 2023
Jul 2023
Historique:
received:
24
02
2023
revised:
05
05
2023
accepted:
12
05
2023
medline:
16
6
2023
pubmed:
23
5
2023
entrez:
23
5
2023
Statut:
ppublish
Résumé
Macrophage M2 polarization has been identified in the pathogenesis of pulmonary fibrosis (PF), but the mediators that drive the macrophage M2 program in PF need to be clarified. We showed that the expression of AMFR and CCR8, two known receptors of CCL1, was increased in macrophages from lungs of mice with bleomycin (BLM)-induced PF. Deficiency in either AMFR or CCR8 in macrophages protected mice from BLM-induced PF. In vitro experiments revealed that CCL1 recruited macrophages by binding to its classical receptor CCR8 and drove the macrophage M2 phenotype via its interaction with the recently identified receptor AMFR. Mechanistic studies revealed that the CCL1-AMFR interaction enhanced CREB/C/EBPβ signaling to promote the macrophage M2 program. Together, our findings reveal that CCL1 acts as a mediator of macrophage M2 polarization and could be a therapeutic target in PF.
Identifiants
pubmed: 37220693
pii: S1567-5769(23)00666-5
doi: 10.1016/j.intimp.2023.110343
pii:
doi:
Substances chimiques
Chemokine CCL1
0
Ccl1 protein, mouse
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
110343Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.