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MpbR, an essential transcriptional factor for Mycobacterium tuberculosis survival in the host, modulates PIM

Yugang Li1, Weihui Li2, Zhiwei Xie1

  • 1National Key Laboratory of Agricultural Microbiology, College of Life Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.

Journal of Genetics and Genomics = Yi Chuan Xue Bao
|January 25, 2020
PubMed

Insights

A newly identified transcriptional factor, MpbR, in Mycobacterium tuberculosis regulates lipid biosynthesis, impacting biofilm formation and enhancing bacterial survival during infection. Its deletion reduces lung inflammation and bacterial load in mice.

Area of Science:

  • Microbiology
  • Immunology
  • Biochemistry

Background:

  • Mycobacterium tuberculosis (M. tuberculosis) has unique cell envelope components aiding immune evasion.
  • Phosphatidylinositol mannosides (PIMs) are crucial lipids in tuberculosis pathogenesis, but their regulatory mechanisms are poorly understood.

Purpose of the Study:

  • To investigate the role of a hypothetical transcriptional factor, MpbR, in regulating M. tuberculosis lipid metabolism and its impact on pathogenesis.
  • To elucidate the effect of MpbR on PIM biosynthesis, biofilm formation, and host-pathogen interactions.

Main Methods:

  • Gene expression analysis of M. tuberculosis transporter genes regulated by MpbR.
  • Analysis of PIM lipid accumulation and reactive oxygen species (ROS) and nitric oxide (NO) production in M. tuberculosis.
  • Assessment of M. tuberculosis survival within macrophages and lung burdens and inflammation in infected mice following MpbR deletion.

Main Results:

  • MpbR negatively regulates two transporter genes, influencing PIM biosynthesis and biofilm formation.
  • MpbR inhibits acylated PIM lipid accumulation, leading to reduced ROS and NO production by M. tuberculosis.
  • MpbR deletion in M. tuberculosis decreased lung bacterial burden and attenuated inflammation in infected mice, enhancing bacterial survival.

Conclusions:

  • MpbR acts as a negative regulator of M. tuberculosis PIM biosynthesis and biofilm formation.
  • MpbR-mediated inhibition of ROS and NO production enhances M. tuberculosis survival in macrophages.
  • Targeting MpbR offers a potential strategy to control M. tuberculosis infection by modulating lipid metabolism and reducing pathogenesis.
Keywords:
Lipid metabolismMycobacterium tuberculosisTranscriptional factor

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