Neumann Silke, Burkert Kristina, Kemp Roslyn, Rades Thomas, Rod Dunbar P, Hook Sarah
1] School of Pharmacy, University of Otago, Dunedin, New Zealand [2] Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand.
1] Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand [2] School of Biological Sciences, University of Auckland, Auckland, New Zealand.
Immunol Cell Biol. 2014 Jul;92(6):535-42. doi: 10.1038/icb.2014.21. Epub 2014 Apr 1.
Particulate vaccine formulations, designed to improve the delivery of antigens to antigen-presenting cells (APCs) and to stimulate an immune response, have been shown to activate the NLRP3 inflammasome. This leads to the processing and secretion of interleukin (IL)-1β, which supports the recruitment of pro-inflammatory immune cells into the tissue and can therefore be beneficial for vaccine potency. Recent work suggested that this may be a common mechanism of action for all particulate formulations. The aim of this study was to investigate whether the activation of the NLRP3 inflammasome was common to many delivery systems. We prepared polymer-based chitosan nanoparticles (CNPs), lipid-based cubosomes, a water in oil emulsion of incomplete Freund's adjuvant (IFA) and alum formulations and examined inflammasome activation in vitro using murine bone-marrow-derived dendritic cells and human peripheral blood mononuclear cells and in vivo in mice. The formulations differed in their morphology, size and zeta-potential. Only the positively charged particles (CNPs and alum) were able to activate the inflammasome and increase the secretion of IL-1β. A decrease in the activation of the inflammasome with these particulates was observed when cathepsin B-mediated effects were blocked, implying a role of lysosomal rupture in the activation process. These findings demonstrate a role for the surface charge of particulates in the activation of the NLRP3 inflammasome, which should be considered when designing a novel vaccine formulation.
旨在改善抗原递送至抗原呈递细胞(APC)并刺激免疫反应的颗粒疫苗制剂已被证明可激活NLRP3炎性小体。这会导致白细胞介素(IL)-1β的加工和分泌,其有助于促炎性免疫细胞募集到组织中,因此对疫苗效力可能有益。最近的研究表明,这可能是所有颗粒制剂的共同作用机制。本研究的目的是调查NLRP3炎性小体的激活是否为许多递送系统所共有。我们制备了基于聚合物的壳聚糖纳米颗粒(CNP)、基于脂质的立方液晶、不完全弗氏佐剂(IFA)的油包水乳剂和明矾制剂,并使用小鼠骨髓来源的树突状细胞和人外周血单核细胞在体外以及在小鼠体内检测炎性小体的激活情况。这些制剂在形态、大小和zeta电位方面存在差异。只有带正电荷的颗粒(CNP和明矾)能够激活炎性小体并增加IL-1β的分泌。当组织蛋白酶B介导的效应被阻断时,观察到这些颗粒对炎性小体激活的降低,这意味着溶酶体破裂在激活过程中起作用。这些发现证明了颗粒表面电荷在NLRP3炎性小体激活中的作用,在设计新型疫苗制剂时应予以考虑。