Genetic variations among genes of Mycobacterium tuberculosis may be associated with antigenic variation and immune evasion, which complicates the pathogenesis of M. tuberculosis. The hyper-virulent M. tuberculosis Beijing strains harbored several large sequence deletions, among which RD207 attributed to the deletion of CRISPR loci and several Cas genes. RD207 also gave rise to a truncated gene Rv2820c-Bj with 60% deletion in length at the 3′-end and a new 3′-end of five amino acid mutations. It has been reported that Rv2820c-Bj correlated with enhanced intracellular survival of M. smegmatis in macrophages when compared to its full-length counterpart Rv2820c in M. tuberculosis, however, the respective contribution of the truncation and the new 3′-end of Rv2820c-Bj to this enhancement was unclear. Here, by infecting THP-1 macrophages with Ms_Rv2820c-Bj, Ms_Rv2820c and MS_Rv2820c-Tr (expressing the truncated Rv2820c without five amino acid mutations at 3′-end), we found only Ms_Rv2820c-Bj was responsible for the enhancement of survival of M. smegmatis in macrophages. Furthermore, we detected that Ms_Rv2820c-Tr and Ms_Rv2820c-Bj induced similar cytokine profile and NO production after infection of macrophages, which was distinctly different from Ms_Rv2820c. However, Ms_Rv2820c-Bj evoked higher levels of interleukin-10 (IL-10) and lower levels of interleukin- 6 (IL-6), interleukin-1β (IL-1β) and interleukin-12 (IL-12) in infected THP-1 macrophages than Ms_Rv2820c-Tr. Accordingly, we concluded that the new 3′-end of Rv2820c-Bj was important to dampen host defense and enhance the intracellular survival of M. smegmatis.
Infection, Genetics and Evolution – Elsevier
Published: Apr 1, 2018
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