Extracellular histones in tissue injury and inflammation.

Détails

ID Serval
serval:BIB_935F8B14A7B7
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Extracellular histones in tissue injury and inflammation.
Périodique
Journal of Molecular Medicine
Auteur(s)
Allam R., Kumar S.V., Darisipudi M.N., Anders H.J.
ISSN
1432-1440 (Electronic)
ISSN-L
0946-2716
Statut éditorial
Publié
Date de publication
2014
Volume
92
Numéro
5
Pages
465-472
Langue
anglais
Résumé
Neutrophil NETosis is an important element of host defense as it catapults chromatin out of the cell to trap bacteria, which then are killed, e.g., by the chromatin's histone component. Also, during sterile inflammation TNF-alpha and other mediators trigger NETosis, which elicits cytotoxic effects on host cells. The same mechanism should apply to other forms of regulated necrosis including pyroptosis, necroptosis, ferroptosis, and cyclophilin D-mediated regulated necrosis. Beyond these toxic effects, extracellular histones also trigger thrombus formation and innate immunity by activating Toll-like receptors and the NLRP3 inflammasome. Thereby, extracellular histones contribute to the microvascular complications of sepsis, major trauma, small vessel vasculitis as well as acute liver, kidney, brain, and lung injury. Finally, histones prevent the degradation of extracellular DNA, which promotes autoimmunization, anti-nuclear antibody formation, and autoimmunity in susceptible individuals. Here, we review the current evidence on the pathogenic role of extracellular histones in disease and discuss how to target extracellular histones to improve disease outcomes.
Mots-clé
Chromatin, Sepsis, Acute kidney injury, Ischemia, DAMP, Neutrophil extracellular traps
Pubmed
Web of science
Création de la notice
15/05/2014 9:10
Dernière modification de la notice
03/03/2018 19:34
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