Utaisincharoen P, Arjcharoen S, Limposuwan K, Tungpradabkul S, Sirisinha S
Department of Microbiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand.
Microb Pathog. 2006 Apr;40(4):184-9. doi: 10.1016/j.micpath.2006.01.002. Epub 2006 Mar 9.
Burkholderia pseudomallei is the causative agent of melioidosis. This bacterium can invade and survive inside the phagocytic and nonphagocytic cells. After internalization, the bacteria can escape from the membrane-bound phagosome into the cytoplasm. Internalised B. pseudomallei can also induce a cell-to-cell fusion, resulting in a multinucleated giant cell (MNGC) formation. In the present study, we demonstrated that B. pseudomallei rpoS null mutant was similar to its wild type parent in its ability to survive and multiply inside the mouse macrophages, but it failed to stimulate MNGC formation. The rpoS mutant was also unable to activate inducible Nitric Oxide Synthase (iNOS) in resting mouse macrophages but in gamma interferon (IFN-gamma)-activated macrophages, the mutant was able to induce significantly higher levels of iNOS and NO when compared with its wild-type counterpart, resulting in a significantly lower number of bacteria inside the infected host cells.
类鼻疽伯克霍尔德菌是类鼻疽的病原体。这种细菌能够侵入吞噬细胞和非吞噬细胞并在其中存活。内化后,细菌可从膜结合吞噬体逃逸至细胞质中。内化的类鼻疽伯克霍尔德菌还可诱导细胞间融合,导致多核巨细胞(MNGC)形成。在本研究中,我们证明类鼻疽伯克霍尔德菌rpoS基因缺失突变体在小鼠巨噬细胞内存活和繁殖的能力与其野生型亲本相似,但它无法刺激MNGC形成。rpoS突变体也无法在静息小鼠巨噬细胞中激活诱导型一氧化氮合酶(iNOS),但在γ干扰素(IFN-γ)激活的巨噬细胞中,与野生型相比,该突变体能够诱导产生显著更高水平的iNOS和NO,导致感染宿主细胞内的细菌数量显著减少。