与野生型结核分枝杆菌相比,devR基因破坏结核分枝杆菌菌株降低C3激活

V. Narayan Rao, S. Manivannan, J. Tyagi, V. D. Ramanathan
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引用次数: 0

摘要

补体成分C3的激活是补体级联反应的重要步骤,有助于炎症机制。利用结核感染动物模型对基因破坏的分枝杆菌菌株进行了大量研究,报道了一些分枝杆菌基因在结核感染中的作用。本研究的目的是评估devR基因破坏的结核分枝杆菌H37Rv菌株的补体激活模式,并与其野生型菌株进行比较。采用固相酶联免疫吸附试验(ELISA)对基因中断菌株、其补充菌株和野生型菌株进行C3水平的体外补体激活。结果发现,devR基因破坏的结核分枝杆菌H37Rv激活C3的能力明显低于其野生型(P < 0.05)。此外,互补的devR突变株对C3的激活几乎与野生菌株相似,这表明C3激活能力的降低可能是由于devR基因的缺失。这些发现表明,基因devR可能有助于补体激活,并有助于结核感染期间的炎症过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Decreased C3 Activation by the devR Gene-Disrupted Mycobacterium tuberculosis Strain in Comparison to the Wild-Type Strain
Activation of the complement component C3 is an important step in the complement cascade, contributing to inflammatory mechanisms. Considerable research on gene-disrupted mycobacterial strains using animal models of tuberculosis infection has reported the roles of some of the mycobacterial genes during tuberculosis infection. The aim of the present study was to assess the pattern of complement activation by the devR gene-disrupted Mycobacterium tuberculosis H37Rv strain and compare with that by its wild-type strain. In vitro complement activation at the level of C3 by the gene-disrupted strain, its complemented strain, and wild-type strain was performed using solid-phase ELISA. It was observed that the ability of devR gene-disrupted M. tuberculosis H37Rv to activate C3 was significantly reduced in comparison to its wild-type strain (P < 0.05). In addition, C3 activation by the complemented devR mutant strain was almost similar to that of the wild strain, which indicated that the reduced ability to activate C3 could potentially be due to the deletion of devR gene. These findings indicate that the gene devR probably aids in complement activation and contributes to the inflammatory processes during tuberculosis infection.
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