Mechanisms of gout inflammation

作者：Ea Hang Korng^*

来源：Presse Medicale, 2011, 40(9): 836-843.

DOI：10.1016/j.lpm.2011.03.016

Gout inflammation is on acute and self-resolving reaction.
MSU crystals con 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-1p (IL-1 beta) and polynuclear neutrophils play central role in gout inflammation.
In vitro, MSU crystal-induced IL-1 beta secretion is secondary mainly to NLRP3. inflammasome activation although numerous proteases are also involved. Mechanisms of NLRP3 in 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-beta) and modification of protein coating on MSU crystal surface.

• 出版日期2011-9