Effect of Mycobacterium tuberculosis higBA on Bacterial Stress Response and Intracellular Infection and Immunity

  Objective  To investigate the effect of Mycobacterium tuberculosis (Mtb) higBA on bacterial stress response and intracellular infection and immunity.

  Methods  The target gene amplified from Mtb H37Rv genome was cloned to the vector and then transferred to Mycobacterium smegmatis (Ms) to construct a recombinant strain. Stress response experiment and Raw264.7 mouse macrophage infection was carried out with Ms_higBA, the recombinant strain, and Ms_ vec, the vector strain. Tests were conducted to measure bacterial colony forming unit (CFU) and transcriptional levels of cytokines, including interleukin (IL)-1β, IL-6, IL-10, IL-12p40, interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and inducible nitric oxide synthase (iNOS).

  Results  The recombinant strain, Ms_higBA, was constructed successfully. According to the findings of the stress response experiment, higBA could indeed enhance bacterial survival under certain conditions of in vitro culture. Intracellular infection experiment demonstrated that higBA enhanced bacterial survival in macrophages and influenced the transcriptional level of cytokines.

  Conclusion  The higBA genes from Mtb play a role in bacterial stress response and intracellular infection and immunity.