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 ( ). 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. 1. Introduction The complement system, comprising more than 30 proteins, represents one of the early components that interact with the pathogen. It contributes to host defense against infection directly by its opsonic, inflammatory, and lytic activities and indirectly by enhancing antibody responses. Complement interacts with mycobacteria during the early stages of infection, during which the bacilli activate the complement system and initiate phagocytosis through C3b opsonisation. Several studies are available that report the activation of complement system by many mycobacterial strains [1–4]. Genetic studies since the past few decades have resulted in a number of genetically modified mycobacterial strains, such as the gene-disrupted or mutant strains [5]. Studies on gene-disrupted strains are very useful in delineating the potential roles of the mycobacterial genes during the process of tuberculosis infection [6, 7]. In this context, various mutant strains were studied in animal models of tuberculosis infection for their pathogenicity and virulence properties [8–10]. However, there is lack of information on the complement activation pattern by these gene-disrupted Mycobacterium tuberculosis strains. Two-component systems play a central role in bacterial adaptation by regulating a spectrum of physiological processes ranging from nutrient uptake
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