Título:	Lysophosphatidylcholine induces NLRP3 inflammasome-mediated foam cell formation and pyroptosis in human monocytes and endothelial cells
Autor(es):	Corrêa, Rafael Silva, Luís Felipe Fonseca Ribeiro, Dalila Juliana Silva Almeida, Raquel das Neves Santos, Igor de Oliveira Corrêa, Luís Henrique Sant'Ana, Lívia Pimentel de Assunção, Leonardo Santos Bozza, Patricia Torres Magalhães, Kelly Grace
Assunto:	Lisofosfolipídio Células adiposas Inflamassoma Aterosclerose
Data de publicação:	2020
Editora:	Frontiers
Referência:	CORRÊA, Rafael et al. Lysophosphatidylcholine induces NLRP3 inflammasome-mediated foam cell formation and pyroptosis in human monocytes and endothelial cells. Frontier in Immunology, v. 10, 2927, 2020. DOI: 10.3389/fimmu.2019.02927. Disponível: https://www.frontiersin.org/articles/10.3389/fimmu.2019.02927/full. Acesso em: 14 maio 2021.
Abstract:	Foam cells are specialized lipid-loaded macrophages derived from monocytes and are a key pathological feature of atherosclerotic lesions. Lysophosphatidylcholine (LPC) is a major lipid component of the plasma membrane with a broad spectrum of proinflammatory activities and plays a key role in atherosclerosis. However, the role of LPC in lipid droplet (LD) biogenesis and the modulation of inflammasome activation is still poorly understood. In the present study, we investigated whether LPC can induce foam cell formation through an analysis of LD biogenesis and determined whether the cell signaling involved in this process is mediated by the inflammasome activation pathway in human endothelial cells and monocytes. Our results showed that LPC induced foam cell formation in both types of cells by increasing LD biogenesis via a NLRP3 inflammasome-dependent pathway. Furthermore, LPC induced pyroptosis in both cells and the activation of the inflammasome with IL-1β secretion, which was dependent on potassium efflux and lysosomal damage in human monocytes. The present study described the IL-1β secretion and foam cell formation triggered by LPC via an inflammasome-mediated pathway in human monocytes and endothelial cells. Our results will help improve our understanding of the relationships among LPC, LD biogenesis, and NLRP3 inflammasome activation in the pathogenesis of atherosclerosis.
Licença:	© 2020 Corrêa, Silva, Ribeiro, Almeida, Santos, Corrêa, Sant'Ana, Assunção, Bozza and Magalhães. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
DOI:	https://doi.org/10.3389/fimmu.2019.02927
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