Inflammasome-induced extracellular vesicles harbour distinct RNA signatures and alter bystander macrophage responses.
Adaptive Immunity
Animals
Biomarkers
/ metabolism
Cell Line
Cells, Cultured
Extracellular Vesicles
/ immunology
Humans
Inflammasomes
/ immunology
Inflammation
/ metabolism
Interferon-beta
/ metabolism
Macrophages
/ immunology
Mice
NLR Family, Pyrin Domain-Containing 3 Protein
/ metabolism
Pyroptosis
RNA
/ analysis
cell communication
extracellular vesicle
inflammasome
inflammation
interferon β
nucleotide‐binding oligomerization domain (NOD)‐containing protein with a pyrin domain (NLRP3)
pyroptosis
Journal
Journal of extracellular vesicles
ISSN: 2001-3078
Titre abrégé: J Extracell Vesicles
Pays: United States
ID NLM: 101610479
Informations de publication
Date de publication:
08 2021
08 2021
Historique:
received:
17
12
2020
revised:
29
06
2021
accepted:
09
07
2021
entrez:
11
8
2021
pubmed:
12
8
2021
medline:
12
8
2021
Statut:
ppublish
Résumé
Infectious organisms and damage of cells can activate inflammasomes, which mediate tissue inflammation and adaptive immunity. These mechanisms evolved to curb the spread of microbes and to induce repair of the damaged tissue. Chronic activation of inflammasomes, however, contributes to non-resolving inflammatory responses that lead to immuno-pathologies. Inflammasome-activated cells undergo an inflammatory cell death associated with the release of potent pro-inflammatory cytokines and poorly characterized extracellular vesicles (EVs). Since inflammasome-induced EVs could signal inflammasome pathway activation in patients with chronic inflammation and modulate bystander cell activation, we performed a systems analysis of the ribonucleic acid (RNA) content and function of two EV classes. We show that EVs released from inflammasome-activated macrophages carry a specific RNA signature and contain interferon β (IFNβ). EV-associated IFNβ induces an interferon signature in bystander cells and results in dampening of NLRP3 inflammasome responses. EVs could, therefore, serve as biomarkers for inflammasome activation and act to prevent systemic hyper-inflammatory states by restricting NLRP3 activation in bystander cells.
Identifiants
pubmed: 34377374
doi: 10.1002/jev2.12127
pii: JEV212127
pmc: PMC8329986
doi:
Substances chimiques
Biomarkers
0
Inflammasomes
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
RNA
63231-63-0
Interferon-beta
77238-31-4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
e12127Informations de copyright
© 2021 The Authors. Journal of Extracellular Vesicles published by Wiley Periodicals, LLC on behalf of the International Society for Extracellular Vesicles.
Déclaration de conflit d'intérêts
Eicke Latz is co‐founder and consultant of IFM Therapeutics. The remaining authors declare no competing interests.
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