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Macrophages lacking lipin-2 enhance IL-1β production through the overactivation of NLRP3 inflammasome

AuthorsLordén, Gema; Balsinde, Jesús ; Balboa, María A.
Issue Date2016
CitationXXXIX Congreso de la SEBBM (2016)
AbstractLipin-2 is a member of the lipin family of proteins, which catalyze the enzymatic conversion of phosphatidic acid to diacylglycerol. Mutations found in the human LPIN2 gene are known to cause Majeed Syndrome, an autoinflammatory disorder in which IL-1βis involved. Since NLRP3 inflammasome orchestrate innate immune responses through activation of caspase-1 leading to the maturation of pro-inflammatory cytokines pro-IL-1β and pro-IL-18, it was hypothesized that lipin-2 could modulate its production and thereby be involved in the regulation of inflammasome activity. We found out that both, classic (LPS and ATP) and metabolic (LPS and palmitic acid) activation of NLRP3 inflammasome, promote an increased production of the proinflammatory cytokine IL-1β in macrophages lacking lipin-2, which depends on the overactivation of NF-κB by LPS. Besides, depletion of lipin-2 in macrophages alter cellular responses to ATP, what leads to overstimulation of the NLRP3 pathway triggering the IL-1β and IL-18 production in an ASC and caspase-1 dependent manner. These effects may be due to the fact that absence of lipin-2 modifies lipid membrane levels, leading to an increase of P2X7 receptor activity, triggering potassium efflux from the cell, and increasing the assembly of the inflammasome and its activity. Collectively, these studies confirm a protective role for lipin-2 in the pathology of inflammatory diseases mediated by activation of inflamasome NLRP3.
DescriptionResumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología Molecular, celebrado en Salamanca del 5 al 8 de septiembre de 2016.
Appears in Collections:(IBGM) Comunicaciones congresos
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