CXCL12 inhibits inflammasome activation in LPS-stimulated BV2 cells.
Animals
Apoptosis Regulatory Proteins
/ metabolism
Calcium-Binding Proteins
/ metabolism
Caspase 1
/ metabolism
Chemokine CXCL12
/ pharmacology
Inflammasomes
/ antagonists & inhibitors
Interleukin-18
/ metabolism
Interleukin-1beta
/ metabolism
Lipopolysaccharides
Mice
Microglia
/ drug effects
NLR Family, Pyrin Domain-Containing 3 Protein
/ metabolism
Receptors, CXCR4
/ metabolism
BV2 cells
CXCL12
Inflammasome
LPS
Spinal cord
Journal
Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503
Informations de publication
Date de publication:
15 07 2021
15 07 2021
Historique:
received:
14
12
2020
revised:
15
03
2021
accepted:
18
03
2021
pubmed:
27
3
2021
medline:
27
1
2022
entrez:
26
3
2021
Statut:
ppublish
Résumé
The activation of the CXCL12-CXCR4 signaling axis is implicated in the regulation of cell survival, proliferation, and mobilization of bone marrow stem cells into the injured site. We have shown in a previous study that intrathecal administration of CXCL12 reduces spinal cord tissue damage and neuroinflammation and provides functional improvement by reducing inflammasome activity and local inflammatory processes in an experimental spinal cord injury (SCI) rat model. Here, we aimed at investigating whether these neuroprotective effects rely on the control of CXCL12 signaling on microglial activation as microglia cells are known to be the primary immune cells of the brain. LPS induced the expression of the inflammasome components NLRP3, NLRC4 and ASC, the secretion of the cytokines IL-1b and IL-18 and the activation of caspase-1 protease in BV2 cells. Pre-treatment with CXCL12 significantly reduced LPS-induced IL-1b/IL-18 secretion and inflammasome induction. Our results also showed that CXCL12 can suppress caspase-1 activity, which leads to a decrease of SCI-related induction of active IL-1b.
Identifiants
pubmed: 33766517
pii: S0006-8993(21)00303-6
doi: 10.1016/j.brainres.2021.147446
pii:
doi:
Substances chimiques
Apoptosis Regulatory Proteins
0
CXCR4 protein, mouse
0
Calcium-Binding Proteins
0
Chemokine CXCL12
0
Inflammasomes
0
Interleukin-18
0
Interleukin-1beta
0
Ipaf protein, mouse
0
Lipopolysaccharides
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Nlrp3 protein, mouse
0
Receptors, CXCR4
0
Caspase 1
EC 3.4.22.36
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
147446Informations de copyright
Copyright © 2021 Elsevier B.V. All rights reserved.