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艾滋病毒感染通过NLRP3炎症细胞激活驱动泡细胞的形成

Maurizio Caocci¹, Meng Niu², Howard S Fox²

¹Department of Microbiology, Immunology, and Inflammation, Center for Neurovirology and Gene Editing, 3500 N Broad St. MERB 760, Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA.

International journal of molecular sciences

|February 24, 2024

概括

在接受抗逆转录病毒治疗 (ART) 的艾滋病毒感染者 (PWH) 中,持续的免疫激活会增加心血管疾病 (CVD) 的风险. 通过促进泡细胞的形成和炎症,NLRP3炎症酶途径有助于增加这种风险.

科学领域:

免疫学免疫学免疫学
心血管科学心血管科学
传染性疾病传染性疾病

背景情况:

持续性免疫激活是接受抗逆转录病毒疗法 (ART) 的HIV感染者 (PWH) 心血管疾病 (CVD) 的已知危险因素.
细胞内蛋白质复合体NLRP3炎症体与炎症过程有关,可能在PWH中观察到的心血管疾病风险增加中发挥作用.

研究的目的:

研究NLRP3炎症酶在艾滋病毒相关心血管疾病中的作用.
探索艾滋病毒感染和NLRP3激活有助于PWH中的动脉动脉生成的机制.

主要方法:

从PWH和HIV阴性对照中分析周围血液单核细胞 (PBMC).
巨细胞和PBMCs的体外HIV感染模型.
RNA测序 (RNAseq) 和途径分析以评估转录变化.
通过使用MCC950.0.抑制NLRP3炎症酶活性.

主要成果:

艾滋病毒感染和oxLDL治疗在巨细胞和PBMC中增加了泡细胞的形成和NLRP3炎症组分 (caspase-1,IL-1β,IL-18) 的表达.
转录组分析揭示了与脂质代谢,胆固醇储存和单细胞/巨细胞功能相关的基因的改变表达.
使用MCC950抑制NLRP3活性,降低了炎症酶激活和泡细胞的形成.
艾滋病毒感染和NLRP3激活与增加的促炎性细胞因子表达有关.

结论:

艾滋病毒感染本身,通过NLRP3炎症酶激活,有助于动脉动脉生成和增加PWH中的心血管疾病风险.
NLRP3炎症酶途径是HIV相关心血管并发症背后的机制的关键参与者.
向NLRP3炎症酶可能是减轻PWH心血管疾病风险的潜在治疗策略.

关键词:

艾滋病病毒艾滋病病毒艾滋病病毒在NLRP3炎症酶组中,这就是为什么PWH是PWH.心血管疾病心血管疾病泡细胞是一种泡细胞.oxLDL oxLDL 的意思是什么?

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