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• W2016558732 abstract "Gout inflammation is an acute and self-resolving reaction. MSU crystals can stimulate cells through either crystal-cell membrane interaction or after their phagocytosis. The onset of gout inflammation relies on non-hematopoietic resident cells whereas the amplification of the reaction is driven by phagocytic cells of immune innate system. Interleukin-1β (IL-1β) and polynuclear neutrophils play central role in gout inflammation. In vitro, MSU crystal-induced IL-1β secretion is secondary mainly to NLRP3 inflammasome activation although numerous proteases are also involved. Mechanisms of NLRP3 inflammasome activation remain unclear involving mostly reactive oxygen species production. Gout resolution involves several mechanisms including monocyte differentiation into macrophage, clearance of apoptotic neutrophils by macrophages, production of Transforming Growth Factor (TGF-β) and modification of protein coating on MSU crystal surface. La réaction inflammatoire déclenchée par les cristaux d’urate monosodique (UMS) est caractérisée par un début brutal et une résolution spontanée. Les cristaux d’UMS activent les cellules, soit via une interaction cristaux-membrane cellulaire, soit après leur phagocytose. L’initiation de l’inflammation dépend des cellules résidentes d’origine non-hématopoïétique et son amplification des cellules phagocytaires de l’immunité innée. L’interleukine-1β (IL-1β) et les polynucléaires neutrophiles occupent une place centrale dans l’inflammation uratique. La production de l’IL-1β in vitro implique l’activation de l’inflammasome NLRP3 selon un mécanisme encore imprécis, probablement dépendant des radicaux libres dérivés de l’oxygène. La résolution de l’inflammation uratique dépend de la clairance des PNN apoptiques, du « switch » des monocytes en macrophages et de la production du Transforming Growth Factor (TGF-β)." @default.
• W2016558732 created "2016-06-24" @default.
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• W2016558732 date "2011-09-01" @default.
• W2016558732 modified "2023-10-16" @default.
• W2016558732 title "Physiopathologie de l’inflammation goutteuse" @default.
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• W2016558732 doi "https://doi.org/10.1016/j.lpm.2011.03.016" @default.
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