Abstract：
Melioidosis, a human infectious disease with a high mortality rate in many tropical countries, is caused by the pathogen Burkholderia pseudomallei (B. pseudomallei). The function of the B. pseudomallei sigma S (RpoS) transcription factor in survival during the stationary growth phase and conditions of oxidative stress is well documented. Besides the rpoS, bioinformatics analysis of B. pseudomallei genome showed the existence of two rpoN genes, named rpoN1 and rpoN2. In this study, by using the mouse macrophage cell line RAW264.7 as a model of infection, the involvement of B. pseudomallei RpoS and RpoN2 in the invasion, intracellular survival leading to the reduction in multinucleated giant cell (MNGC) formation of RAW264.7 cell line were illustrated. We have demonstrated that the MNGC formation of RAW264.7 cell was dependent on a certain number of intracellular bacteria (at least 5 × 104). In addition, the same MNGC formation (15%) observed in RAW264.7 cells infected with either B. pseudomallei wild type with multiplicity of infection (MOI) 2 or RpoN2 mutant (∆rpoN2) with MOI 10 or RpoS mutant (∆rpoS) with MOI 100. The role of B. pseudomallei RpoS and RpoN2 in the regulation of type III secretion system on bipB-bipC gene expression was also illustrated in this study.
摘要：
类粘液病,一种在许多热带国家死亡率很高的人类传染病，是由病原体假伯克霍尔德氏菌(B.pseudomallei).在稳态生长期和氧化应激条件下，假单胞菌sigmaS（RpoS）转录因子在存活中的功能已得到充分证明。除了rpos,假单胞菌基因组的生物信息学分析显示存在两个rpoN基因，命名为rpoN1和rpoN2。在这项研究中,通过使用小鼠巨噬细胞系RAW264.7作为感染模型，假单胞菌RpoS和RpoN2参与入侵，说明了导致RAW264.7细胞系多核巨细胞（MNGC）形成减少的细胞内存活。我们已经证明，RAW264.7细胞的MNGC形成取决于一定数量的细胞内细菌（至少5×104）。此外,在RAW264.7细胞中观察到相同的MNGC形成（15％），这些细胞感染了具有感染复数（MOI）2的假单胞菌野生型或具有MOI10的RpoN2突变体（取决于rpoN2）或具有MOI100的RpoS突变体（取决于rpoS）。本研究还阐明了假单胞菌RpoS和RpoN2在III型分泌系统对bipB-bipC基因表达的调节中的作用。
