Cutting edge: cyclic polypeptide and aminoglycoside antibiotics trigger IL-1β secretion by activating the NLRP3 inflammasome.

Détails

ID Serval
serval:BIB_849E5AFB9646
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Cutting edge: cyclic polypeptide and aminoglycoside antibiotics trigger IL-1β secretion by activating the NLRP3 inflammasome.
Périodique
Journal of Immunology
Auteur(s)
Allam R., Darisipudi M.N., Rupanagudi K.V., Lichtnekert J., Tschopp J., Anders H.J.
ISSN
1550-6606 (Electronic)
ISSN-L
0022-1767
Statut éditorial
Publié
Date de publication
2011
Volume
186
Numéro
5
Pages
2714-2718
Langue
anglais
Résumé
Clinical use of antibiotics is based on their capacity to inhibit bacterial growth via bacteriostatic or bacteriocidal effects. In this article, we show that the aminoglycoside antibiotic neomycin, the cyclic lipopeptide antibiotic polymyxin B, and the cyclic peptide antibiotics gramicidin and tyrothricin can induce IL-1β secretion in bone marrow dendritic cells and macrophages. LPS priming was required to trigger the transcription and translation of pro-IL-1β but was independent of TNFR or IL-1R signaling. All four antibiotics required the NLRP3 inflammasome, the adaptor ASC, and caspase-1 activation to secrete IL-1β, a process that depended on potassium efflux but was independent of P2X7 receptor. All four antibiotics induced neutrophil influx into the peritoneal cavity of mice, which required NLRP3 only in the case of polymyxin B. Together, certain antibiotics have the potential to directly activate innate immunity of the host.
Mots-clé
Aminoglycosides/pharmacology, Animals, Anti-Bacterial Agents/pharmacology, Bone Marrow Cells/drug effects, Bone Marrow Cells/immunology, Carrier Proteins/genetics, Carrier Proteins/metabolism, Dendritic Cells/immunology, Dendritic Cells/metabolism, Humans, Inflammasomes/genetics, Inflammasomes/metabolism, Interleukin-1beta/biosynthesis, Interleukin-1beta/secretion, Macrophage Activation/drug effects, Macrophage Activation/immunology, Macrophages, Peritoneal/immunology, Macrophages, Peritoneal/metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Peptides, Cyclic/pharmacology, Peritonitis/immunology, Peritonitis/metabolism, Protein Precursors/biosynthesis, Protein Precursors/secretion, Receptors, Interleukin-1/deficiency, Receptors, Interleukin-1/genetics
Pubmed
Web of science
Open Access
Oui
Création de la notice
02/09/2011 10:00
Dernière modification de la notice
08/05/2019 21:20
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