a Centre d'Immunologie de Marseille-Luminy, CIML, Aix Marseille Univ, CNRS, INSERM , Marseille , France.
b Departamento de Microbiología y Parasitología , Instituto de Salud Tropical, Instituto de Investigación Sanitaria de Navarra, Universidad de Navarra , c/Irunlarrea 1, Pamplona , Spain.
Virulence. 2018 Jan 1;9(1):465-479. doi: 10.1080/21505594.2017.1386831.
The lipopolysaccharide (LPS) is a major virulence factor of Brucella, a facultative intracellular pathogenic Gram-negative bacterium. Brucella LPS exhibits a low toxicity and its atypical structure was postulated to delay the host immune response, favouring the establishment of chronic disease. Here we carried out an in-depth in vitro and in vivo characterisation of the immunomodulatory effects of Brucella LPS on different dendritic cell (DC) subpopulations. By using LPSs from bacteria that share some of Brucella LPS structural features, we demonstrated that the core component of B. melitensis wild-type (Bm-wt) LPS accounts for the low activation potential of Brucella LPS in mouse GM-CSF-derived (GM-) DCs. Contrary to the accepted dogma considering Brucella LPS a poor TLR4 agonist and DC activator, Bm-wt LPS selectively induced expression of surface activation markers and cytokine secretion from Flt3-Ligand-derived (FL-) DCs in a TLR4-dependent manner. It also primed in vitro T cell proliferation by FL-DCs. In contrast, modified LPS with a defective core purified from Brucella carrying a mutated wadC gene (Bm-wadC), efficiently potentiated mouse and human DC activation and T cell proliferation in vitro. In vivo, Bm-wt LPS promoted scant activation of splenic DC subsets and limited recruitment of monocyte- DC like cells in the spleen, conversely to Bm-wadC LPS. Bm-wadC live bacteria drove high cytokine secretion levels in sera of infected mice. Altogether, these results illustrate the immunomodulatory properties of Brucella LPS and the enhanced DC activation ability of the wadC mutation with potential for vaccine development targeting Brucella core LPS structure.
脂多糖(LPS)是布鲁氏菌的主要毒力因子,布鲁氏菌是一种兼性胞内致病性革兰氏阴性菌。布鲁氏菌 LPS 表现出低毒性,其非典型结构被推测为延迟宿主免疫反应,有利于慢性疾病的建立。在这里,我们对布鲁氏菌 LPS 对不同树突状细胞(DC)亚群的免疫调节作用进行了深入的体外和体内研究。通过使用与布鲁氏菌 LPS 具有某些结构特征的细菌 LPS,我们证明了 B. melitensis 野生型(Bm-wt)LPS 的核心成分解释了布鲁氏菌 LPS 在小鼠 GM-CSF 衍生(GM-)DC 中低激活潜能的原因。与认为布鲁氏菌 LPS 是 TLR4 激动剂和 DC 激活剂较差的公认观点相反,Bm-wt LPS 以 TLR4 依赖的方式选择性诱导 Flt3-Ligand 衍生(FL-)DC 表面激活标志物的表达和细胞因子的分泌。它还通过 FL-DC 体外刺激 T 细胞增殖。相比之下,从携带突变 wadC 基因的布鲁氏菌中纯化的具有缺陷核心的修饰 LPS(Bm-wadC)有效地增强了小鼠和人 DC 的体外激活和 T 细胞增殖。在体内,Bm-wt LPS 促进了脾脏 DC 亚群的激活和脾脏中单核细胞样 DC 的募集,与 Bm-wadC LPS 相反。Bm-wadC 活菌在感染小鼠的血清中驱动高水平的细胞因子分泌。总之,这些结果说明了布鲁氏菌 LPS 的免疫调节特性,以及 wadC 突变增强了 DC 激活能力,这为针对布鲁氏菌核心 LPS 结构的疫苗开发提供了潜力。