ABSTRACT
Mycobacterium tuberculosis can manipulate the host immunity through its effectors to ensure intracellular survival and colonization. Rv1043c has been identified as an effector potentially involved in M. tuberculosis pathogenicity. To explore the function of M. tuberculosis Rv1043c during infection, we overexpressed this protein in M. smegmatis, a non-pathogenic surrogate model in tuberculosis research. Here, we reported that Rv1043c enhanced mycobacterial survival and down-regulated the release of pro-inflammatory cytokines in macrophages and mice. In addition, Rv1043c inhibited the activation of MAPK and NF-κB signaling by preventing the phosphorylation of TAK1 indirectly. In conclusion, these data suggest that Rv1043c regulates the immune response and enhances the survival of recombinant M. smegmatis in vitro and in vivo.
ABSTRACT
The distinctive cell walls of mycobacteria are characteristic features of these bacteria. Individual cell wall components influence diverse mycobacterial phenotypes, such as colony morphology, virulence and stress resistance. To investigate the role of the hypothetical protein Rv2387, we constructed a Mycobacterium smegmatis strain that heterologously expressed this ORF, and we observed that the M. smegmatis strain expressing Rv2387 exhibited altered colony morphology and cell wall lipid composition, leading to a marked decrease in the resistance against acidic conditions. This study demonstrates that due to its impact on cell wall remodeling, Rv2387 might play an important role in mycobacterial physiology.
