Abstract：
The co-evolution of Mycobacterium tuberculosis H37Rv along with its host systems enables the pathogenic bacterium to emerge as a multi-drug resistant form. This creates challenges for a more efficacious treatment strategy that can mitigate the infection. Working towards the same, our study followed a mathematical and statistical approach proposing that mycobacterial transcription factors regulating virulence and adaptation, host cell cytoplasmic component metabolism, oxidoreductase activity and respiratory ETC would be targets for antibiotics against Mycobacterium tuberculosis. Simultaneously, extending the statistical study on Mycobacterium-infected human cord blood CD34+ cells revealed that the human CD34+ genes, S100A8 and FGR (tyrosine-protein kinase, Src2), might be affected in the infection pathogenesis by Mycobacterium. Further, the deduced Mycobacterium-human gene interaction network proposed that mycobacterial coregulators Rv0452 (MarR family regulator) and Rv3862c (WhiB6) triggered genes controlling bacterial metabolism, which influences human immunological pathways involving TLR2 and CXCL8/MAPK8.Communicated by Ramaswamy H. Sarma.
摘要：
结核分枝杆菌H37Rv及其宿主系统的共同进化使致病细菌能够以多重耐药形式出现。这对可以减轻感染的更有效的治疗策略产生了挑战。朝着同样的方向努力，我们的研究遵循数学和统计方法，提出分枝杆菌转录因子调节毒力和适应性，宿主细胞细胞质成分代谢，氧化还原酶活性和呼吸道ETC将成为抗结核分枝杆菌抗生素的靶标。同时,扩展对分枝杆菌感染的人脐带血CD34+细胞的统计研究表明，人CD34+基因，S100A8和FGR（酪氨酸蛋白激酶，Src2),可能在分枝杆菌的感染发病机制中受到影响。Further,推导的分枝杆菌-人类基因相互作用网络提出分枝杆菌共调节因子Rv0452（MarR家族调节因子）和Rv3862c（WhiB6）触发控制细菌代谢的基因，影响涉及TLR2和CXCL8/MAPK8的人类免疫途径。由RamaswamyH.Sarma沟通。
