Rachman Helmy, Strong Michael, Schaible Ulrich, Schuchhardt Johannes, Hagens Kristine, Mollenkopf Hans, Eisenberg David, Kaufmann Stefan H E
Max Planck Institute for Infection Biology, Department of Immunology, Schumannstrasse 21-22, 10117 Berlin, Germany.
Microbes Infect. 2006 Mar;8(3):747-57. doi: 10.1016/j.micinf.2005.09.011. Epub 2006 Jan 18.
As one of the world's most successful intracellular pathogens, Mycobacterium tuberculosis, the causative agent of human tuberculosis, is responsible for two to three million deaths annually. The pathogenicity of M. tuberculosis relies on its ability to survive and persist within host macrophage cells during infection. It is of central importance, therefore, to identify genes and pathways that are involved in the survival and persistence of M. tuberculosis within these cells. Utilizing genome-wide DNA arrays we have identified M. tuberculosis genes that are specifically induced during macrophage infection. To better understand the cellular context of these differentially expressed genes, we have also combined our array analyses with computational methods of protein network identification. Our combined approach reveals certain signatures of M. tuberculosis residing within macrophage cells, including the induction of genes involved in DNA damage repair, fatty acid degradation, iron metabolism, and cell wall metabolism.
作为世界上最成功的细胞内病原体之一,结核分枝杆菌是人类结核病的病原体,每年导致两到三百万人死亡。结核分枝杆菌的致病性依赖于其在感染期间在宿主巨噬细胞内存活和持续存在的能力。因此,识别参与结核分枝杆菌在这些细胞内存活和持续存在的基因和途径至关重要。利用全基因组DNA阵列,我们已经鉴定出在巨噬细胞感染期间特异性诱导的结核分枝杆菌基因。为了更好地理解这些差异表达基因的细胞背景,我们还将阵列分析与蛋白质网络识别的计算方法相结合。我们的综合方法揭示了结核分枝杆菌存在于巨噬细胞内的某些特征,包括参与DNA损伤修复、脂肪酸降解、铁代谢和细胞壁代谢的基因的诱导。