Roles of CCR2 and CCR5 for Hepatic Macrophage Polarization in Mice With Liver Parenchymal Cell-Specific NEMO Deletion.
Animals
Carcinogenesis
/ immunology
Cells, Cultured
Disease Models, Animal
Disease Progression
Hepatitis
/ immunology
Hepatocytes
/ immunology
Humans
Intracellular Signaling Peptides and Proteins
/ genetics
Liver
/ cytology
Liver Cirrhosis
/ immunology
Liver Neoplasms
/ immunology
Macrophages
/ immunology
Male
Mice
Mice, Knockout
Primary Cell Culture
Receptors, CCR2
/ genetics
Receptors, CCR5
/ genetics
Cell Therapy
Hepatitis
Liver Cancer
Macrophages
Journal
Cellular and molecular gastroenterology and hepatology
ISSN: 2352-345X
Titre abrégé: Cell Mol Gastroenterol Hepatol
Pays: United States
ID NLM: 101648302
Informations de publication
Date de publication:
2021
2021
Historique:
received:
16
02
2020
revised:
27
08
2020
accepted:
31
08
2020
pubmed:
9
9
2020
medline:
21
12
2021
entrez:
8
9
2020
Statut:
ppublish
Résumé
Macrophages are key regulators of inflammation and cancer promotion in the liver, and their recruitment and activation is linked to chemokine receptor signaling. However, the exact roles of the chemokine receptors CCR2 and CCR5 for macrophage functions in the liver is obscure. To study CCR2 and CCR5 in inflammatory liver injury, we used mice with a hepatocyte-specific knock-out of the nuclear factor κB (NF-κB) essential modulator (NEMO), termed NEMO We found that both CCR2 and CCR5 deficiency led to reduced fibrosis, while CCR5 deficiency increased steatosis and tumor burden in NEMO Although CCR2 and CCR5 principally promote liver fibrosis, they exert differential functions on hepatic macrophages during liver disease progression in NEMO
Sections du résumé
BACKGROUND & AIMS
Macrophages are key regulators of inflammation and cancer promotion in the liver, and their recruitment and activation is linked to chemokine receptor signaling. However, the exact roles of the chemokine receptors CCR2 and CCR5 for macrophage functions in the liver is obscure.
METHODS
To study CCR2 and CCR5 in inflammatory liver injury, we used mice with a hepatocyte-specific knock-out of the nuclear factor κB (NF-κB) essential modulator (NEMO), termed NEMO
RESULTS
We found that both CCR2 and CCR5 deficiency led to reduced fibrosis, while CCR5 deficiency increased steatosis and tumor burden in NEMO
CONCLUSIONS
Although CCR2 and CCR5 principally promote liver fibrosis, they exert differential functions on hepatic macrophages during liver disease progression in NEMO
Identifiants
pubmed: 32896623
pii: S2352-345X(20)30136-3
doi: 10.1016/j.jcmgh.2020.08.012
pmc: PMC7779787
pii:
doi:
Substances chimiques
CCR5 protein, mouse
0
Ccr2 protein, mouse
0
Intracellular Signaling Peptides and Proteins
0
NEMO protein, mouse
0
Receptors, CCR2
0
Receptors, CCR5
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
327-347Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.