莱什马尼亚巴西尼斯的外体激活人类的巨细胞,产生促炎媒介体
Fabio C Peixoto1,2, Dalila L Zanette3, Thiago M Cardoso1
1Laboratório de Pesquisas Clínicas (LAPEC), Instituto Gonçalo Moniz (IGM), Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia, Brazil.
Frontiers in immunology
|October 16, 2023
概括
莱什马尼亚巴西人外体是主要的巨细胞,产生炎症性细胞因子,可能会加剧莱什马尼亚病. 这种外体诱导的炎症似乎依赖于NLRP3炎症途径.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 寄生虫学的寄生虫学
背景情况:
- 外体是细胞分泌的纳米级囊泡,携带蛋白质,mRNA和miRNA.
- 莱什曼尼亚外体可以调节宿主免疫反应,促进寄生虫的生存.
- 巨细胞可以表现出训练有素的免疫力,改变对后续刺激的反应.
研究的目的:
- 为了研究莱什马尼亚巴西人外体敏感化对感染前人类巨细胞反应的影响.
- 阐明NLRP3炎症酶在外酶介导的巨细胞激活中的作用.
主要方法:
- 人类巨细胞被L. braziliensis外体刺激.
- 敏感化的巨细胞随后被L. braziliensis感染.
- 分析了细胞因子水平 (IL-1β,IL-6,IL-10,TNF) 和NLRP3炎症组分.
- 评估了NLRP3炎症酶阻断的作用.
主要成果:
- 与对照组相比,外体敏感化的巨细胞产生了较高水平的IL-1β和IL-6.
- 在L. braziliensis外基因组中诱导巨细胞产生IL-1β,IL-6,IL-10和TNF.
- 抑制外体分泌减少了细胞因子的产生和感染率.
- 外体刺激导致NLRP3炎症组分的调节;NLRP3阻断降低了IL-6和IL-1β.
结论:
- L. braziliensis外体刺激巨细胞,导致炎症状态加剧.
- 这种外体驱动的炎症可能由NLRP3炎症体介导.
- 外体体在莱什马尼亚感染期间调节宿主-病原体相互作用方面发挥着重要作用.
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