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伯克霍尔德菌假鼻疽杆菌毒力基因表达调控因子BPSS1521(bprD)在小鼠模型中的特性分析

Characterization of BPSS1521 (bprD), a regulator of Burkholderia pseudomallei virulence gene expression in the mouse model.

作者信息

Chirakul Sunisa, Bartpho Thanatchaporn, Wongsurawat Thidathip, Taweechaisupapong Suwimol, Karoonutaisiri Nitsara, Talaat Adel M, Wongratanacheewin Surasakdi, Ernst Robert K, Sermswan Rasana W

机构信息

Melioidosis Research Center, Khon Kaen University, Khon Kaen, Thailand; Department of Biochemistry, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.

Melioidosis Research Center, Khon Kaen University, Khon Kaen, Thailand.

出版信息

PLoS One. 2014 Aug 11;9(8):e104313. doi: 10.1371/journal.pone.0104313. eCollection 2014.

Abstract

The Gram-negative saprophytic bacterium Burkholderia pseudomallei is the causative agent of melioidosis, a severe infectious disease of both humans and animals. Severity of the disease is thought to be dependent on both the health status of the host, including diabetes mellitus and kidney disease, and bacterial-derived factors. To identify the bacterial factors important during an acute infection, gene expression profiles in the spleen, lung, and liver of BALB/c (Th2 prototype) and C57BL/6 mice (Th1 prototype) were determined using DNA microarrays. This analysis identified BPSS1521 (bprD), a predicted transcriptional regulator located in the type III secretion system (T3SS-3) operon, to be up regulated, specifically in C57BL/6 mice. BALB/c mice infected with a bprD mutant showed a shorter time to death and increased inflammation, as determined by histopathological analysis and enumeration of bacteria in the spleen. Elevated numbers of multinucleated giant cells (MNGCs), which is the hallmark of melioidosis, were detected in both the wild-type and the bprD mutants; a similar elevation occurs in melioidosis patients. One striking observation was the increased expression of BPSS1520 (bprC), located downstream of bprD, in the bprD mutant. BprC is a regulator of T6SS-1 that is required for the virulence of B. pseudomallei in murine infection models. Deletion of bprD led to the overexpression of bprC and a decreased time to death. bprD expression was elevated in C57BL/6--as compared to BALB/c--mice, suggesting a role for BprD in the natural resistance of C57BL/6 mice to B. pseudomallei. Ultimately, this analysis using mice with different immune backgrounds may enhance our understanding of the outcomes of infection in a variety of models.

摘要

革兰氏阴性腐生菌伯克霍尔德菌是类鼻疽的病原体,类鼻疽是一种人和动物都会感染的严重传染病。该疾病的严重程度被认为既取决于宿主的健康状况,包括糖尿病和肾脏疾病,也取决于细菌衍生的因素。为了确定急性感染期间重要的细菌因素,使用DNA微阵列测定了BALB/c(Th2原型)和C57BL/6小鼠(Th1原型)的脾脏、肺和肝脏中的基因表达谱。该分析确定位于III型分泌系统(T3SS-3)操纵子中的预测转录调节因子BPSS1521(bprD)被上调,特别是在C57BL/6小鼠中。感染bprD突变体的BALB/c小鼠死亡时间缩短,炎症增加,这通过组织病理学分析和脾脏中细菌计数确定。在野生型和bprD突变体中均检测到多核巨细胞(MNGC)数量增加,这是类鼻疽的标志;类鼻疽患者也会出现类似的增加。一个显著的观察结果是,位于bprD下游的BPSS1520(bprC)在bprD突变体中的表达增加。BprC是T6SS-1的调节因子,在小鼠感染模型中,它是伯克霍尔德菌毒力所必需的。bprD的缺失导致bprC的过表达和死亡时间缩短。与BALB/c小鼠相比,bprD在C57BL/6小鼠中的表达升高,这表明BprD在C57BL/6小鼠对伯克霍尔德菌的天然抗性中发挥作用。最终,使用具有不同免疫背景的小鼠进行的这项分析可能会增强我们对各种模型中感染结果的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c1d/4128674/bc4fc65b9b1d/pone.0104313.g001.jpg

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