Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Cell Death Dis. 2011 Mar 31;2(3):e137. doi: 10.1038/cddis.2011.18.
The interleukin-1 (IL-1) family of cytokines has been implicated in the pathogenesis of atherosclerosis in previous studies. The NLRP3 inflammasome has recently emerged as a pivotal regulator of IL-1β maturation and secretion by macrophages. Little is currently known about a possible role for the NLRP3 inflammasome in atherosclerosis progression in vivo. We generated ApoE-/- Nlrp3-/-, ApoE-/- Asc-/- and ApoE-/- caspase-1-/- double-deficient mice, fed them a high-fat diet for 11 weeks and subsequently assessed atherosclerosis progression and plaque phenotype. No differences in atherosclerosis progression, infiltration of plaques by macrophages, nor plaque stability and phenotype across the genotypes studied were found. Our results demonstrate that the NLRP3 inflammasome is not critically implicated in atherosclerosis progression in the ApoE mouse model.
白细胞介素-1 (IL-1) 家族细胞因子在先前的研究中被认为与动脉粥样硬化的发病机制有关。NLRP3 炎性小体最近被认为是巨噬细胞中 IL-1β 成熟和分泌的关键调节因子。目前对于 NLRP3 炎性小体在体内动脉粥样硬化进展中的可能作用知之甚少。我们生成了 ApoE-/-Nlrp3-/-、ApoE-/-Asc-/-和 ApoE-/-caspase-1-/-双重基因敲除小鼠，用高脂肪饮食喂养它们 11 周，然后评估动脉粥样硬化的进展和斑块表型。在研究的基因型中，没有发现动脉粥样硬化进展、斑块内巨噬细胞浸润以及斑块稳定性和表型的差异。我们的结果表明，NLRP3 炎性小体在 ApoE 小鼠模型中并不严重参与动脉粥样硬化的进展。
