Membrane-bound Interleukin-1α mediates leukocyte adhesion during atherogenesis.
atherosclerosis
hyperlipidemia
inflammation
interleukin - 1
mouse model
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2023
2023
Historique:
received:
04
07
2023
accepted:
10
08
2023
medline:
14
9
2023
pubmed:
13
9
2023
entrez:
13
9
2023
Statut:
epublish
Résumé
The interleukin-1 (IL-1) family and the NLR family pyrin domain-containing 3 (NLRP3) inflammasome contribute to atherogenesis but the underlying mechanisms are incompletely understood. Unlike IL-1β, IL-1α is not dependent on the NLRP3 inflammasome to exert its pro-inflammatory effects. Here, a non-genetic model was applied to characterize the role of IL-1α, IL-1β, and NLRP3 for the pathogenesis of atherosclerosis. Atherogenesis was induced by gain-of-function PCSK9-AAV8 mutant viruses and feeding of a high-fat western diet (WTD) for 12 weeks in C57Bl6/J wildtype mice (WT) and in Il1a PCSK9-Il1a The results highlight the importance of IL-1α on the cell surface of circulating leucocytes for the development of atherosclerosis. PCSK9-Il1a
Identifiants
pubmed: 37701434
doi: 10.3389/fimmu.2023.1252384
pmc: PMC10494239
doi:
Substances chimiques
Inflammasomes
0
Interleukin-1alpha
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Il1a protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1252384Informations de copyright
Copyright © 2023 Maeder, Speer, Wirth, Boeckel, Fatima, Shahzad, Freichel, Laufs and Gaul.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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