ATP Release Drives Inflammation with Lysophosphatidylcholine.
Adenosine Triphosphate
/ immunology
Animals
Cells, Cultured
Endothelial Cells
/ metabolism
Humans
Inflammation
/ metabolism
Interleukin-12
/ metabolism
Interleukin-1beta
/ metabolism
Lysophosphatidylcholines
/ pharmacology
Macrophages
/ metabolism
Mice
Mice, Inbred C57BL
Neurons
/ metabolism
Signal Transduction
/ drug effects
THP-1 Cells
Journal
ImmunoHorizons
ISSN: 2573-7732
Titre abrégé: Immunohorizons
Pays: United States
ID NLM: 101708159
Informations de publication
Date de publication:
28 04 2021
28 04 2021
Historique:
received:
08
03
2021
accepted:
17
03
2021
entrez:
29
4
2021
pubmed:
30
4
2021
medline:
1
2
2022
Statut:
epublish
Résumé
Lysophosphatidylcholine (LPC), a dominant lipid component of oxidized low-density lipoprotein, plays a major role in inflammation associated with atherosclerosis and neurodegenerative disorders. It activates inflammatory responses from macrophages, neuronal cells, and endothelial cells. However, the exact mechanism by which LPC promotes inflammation remains incompletely understood. In this study, we show that the production of inflammatory cytokines and cytotoxicity with LPC are both critically dependent on its ability to bring about release of ATP from cells. The induction of caspase-1-mediated IL-1β release with LPC from TLR-primed mouse and human macrophages and mouse neuronal cells is reduced in the presence of ATP-hydrolyzing enzyme, apyrase, and the inhibitors of purinergic signaling. ATP released from LPC-treated cells also promotes an IL-12p70
Identifiants
pubmed: 33911018
pii: immunohorizons.2100023
doi: 10.4049/immunohorizons.2100023
doi:
Substances chimiques
Interleukin-1beta
0
Lysophosphatidylcholines
0
Interleukin-12
187348-17-0
Adenosine Triphosphate
8L70Q75FXE
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
219-233Informations de copyright
Copyright © 2021 The Authors.