Papadopoulos Alexia, Gagnaire Aurélie, Degos Clara, de Chastellier Chantal, Gorvel Jean-Pierre
a Centre d'Immunologie de Marseille-Luminy; Aix Marseille Université; CNRS UMR7280; INSERM U1104 ; Marseille , France.
Virulence. 2016;7(1):33-44. doi: 10.1080/21505594.2015.1108516. Epub 2015 Nov 25.
Brucella is a Gram-negative bacterium responsible for brucellosis, a worldwide re-emerging zoonosis. Brucella has been shown to infect and replicate within Granulocyte macrophage colony-stimulating factor (GMCSF) in vitro grown bone marrow-derived dendritic cells (BMDC). In this cell model, Brucella can efficiently control BMDC maturation. However, it has been shown that Brucella infection in vivo induces spleen dendritic cells (DC) migration and maturation. As DCs form a complex network composed by several subpopulations, differences observed may be due to different interactions between Brucella and DC subsets. Here, we compare Brucella interaction with several in vitro BMDC models. The present study shows that Brucella is capable of replicating in all the BMDC models tested with a high infection rate at early time points in GMCSF-IL15 DCs and Flt3l DCs. GMCSF-IL15 DCs and Flt3l DCs are more activated than the other studied DC models and consequently intracellular bacteria are not efficiently targeted to the ER replicative niche. Interestingly, GMCSF-DC and GMCSF-Flt3l DC response to infection is comparable. However, the key difference between these 2 models concerns IL10 secretion by GMCSF DCs observed at 48 h post-infection. IL10 secretion can explain the weak secretion of IL12p70 and TNFα in the GMCSF-DC model and the low level of maturation observed when compared to GMCSF-IL15 DCs and Flt3l DCs. These models provide good tools to understand how Brucella induce DC maturation in vivo and may lead to new therapeutic design using DCs as cellular vaccines capable of enhancing immune response against pathogens.
布鲁氏菌是一种革兰氏阴性细菌,可引发布鲁氏菌病,这是一种在全球范围内再度出现的人畜共患病。已证明布鲁氏菌可在体外培养的粒细胞巨噬细胞集落刺激因子(GMCSF)诱导的骨髓来源树突状细胞(BMDC)内感染并复制。在这个细胞模型中,布鲁氏菌能够有效控制BMDC的成熟。然而,研究表明,布鲁氏菌在体内感染会诱导脾脏树突状细胞(DC)迁移和成熟。由于DC形成了一个由多个亚群组成的复杂网络,观察到的差异可能是由于布鲁氏菌与DC亚群之间的不同相互作用所致。在此,我们比较了布鲁氏菌与几种体外BMDC模型的相互作用。本研究表明,布鲁氏菌能够在所有测试的BMDC模型中复制,在GMCSF-IL15 DCs和Flt3l DCs的早期时间点感染率很高。GMCSF-IL15 DCs和Flt3l DCs比其他研究的DC模型更具活性,因此细胞内细菌不能有效地靶向内质网复制位点。有趣的是,GMCSF-DC和GMCSF-Flt3l DC对感染的反应相当。然而,这两种模型之间的关键差异在于感染后48小时观察到的GMCSF DCs分泌的IL10。IL10的分泌可以解释GMCSF-DC模型中IL12p70和TNFα的微弱分泌,以及与GMCSF-IL15 DCs和Flt3l DCs相比观察到的低水平成熟。这些模型为理解布鲁氏菌如何在体内诱导DC成熟提供了良好的工具,并可能导致使用DC作为细胞疫苗的新治疗设计,从而增强针对病原体的免疫反应。