Kang Wen-Tyng, Vellasamy Kumutha Malar, Chua Eng-Guan, Vadivelu Jamuna
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
J Infect Dis. 2015 Mar 1;211(5):827-34. doi: 10.1093/infdis/jiu492. Epub 2014 Aug 26.
The bsa locus of Burkholderia pseudomallei encodes several proteins that are components of the type III secretion system (TTSS). BipC was postulated as one of the TTSS-3 effector proteins, but its role in the pathogenesis of B. pseudomallei infection is not well understood. Thus, the aim of this study was to determine its role(s) in the virulence of B. pseudomallei pathogenesis.
A bipC TTSS-3-deficient strain of B. pseudomallei and complemented strains were generated to assess the role of BipC as a type III translocation apparatus. Human cell lines and a mouse model of melioidosis were used for in vitro and in vivo assays, respectively.
A significant 2-fold reduction was demonstrated in the percentage of adherence, invasion, intracellular survival, and phagosomal escape of the bipC mutant. Interestingly, microscopic studies have shown that BipC was capable of delayed B. pseudomallei actin-based motility. The virulence of the mutant strain in a murine model of melioidosis demonstrated that the bipC mutant was less virulent, compared with the wild type.
The results suggested that BipC possesses virulence determinants that play significant roles in host cell invasion and immune evasion.
类鼻疽伯克霍尔德菌的bsa基因座编码几种作为III型分泌系统（TTSS）组分的蛋白质。BipC被假定为TTSS-3效应蛋白之一，但其在类鼻疽伯克霍尔德菌感染发病机制中的作用尚不清楚。因此，本研究的目的是确定其在类鼻疽伯克霍尔德菌发病机制毒力中的作用。
构建了类鼻疽伯克霍尔德菌的bipC TTSS-3缺陷菌株和互补菌株，以评估BipC作为III型转运装置的作用。分别使用人细胞系和类鼻疽病小鼠模型进行体外和体内试验。
bipC突变体的黏附、侵袭、细胞内存活和吞噬体逃逸百分比显著降低了2倍。有趣的是，显微镜研究表明，BipC能够延迟类鼻疽伯克霍尔德菌基于肌动蛋白的运动。在类鼻疽病小鼠模型中，突变株的毒力表明，与野生型相比，bipC突变体的毒力较低。
结果表明，BipC具有在宿主细胞侵袭和免疫逃避中起重要作用的毒力决定因素。
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