Human tuberculosis brain promotes neuronal apoptosis but not in astrocytes with high expression of vascular endothelial growth factor

Tuberculosis (Edinb). 2018 Sep:112:45-51. doi: 10.1016/j.tube.2018.07.007. Epub 2018 Jul 18.

Abstract

The present study aimed to investigate the involvement of the angiogenic marker vascular endothelia growth factor (VEGF) and apoptotic markers of Bcl-2 and Bax in the neurons and astrocytes in the brain infected by Mycobacterium tuberculosis. The immunohistochemistry staining was performed to analyze the expression of the VEGF, Bcl-2 and Bax in the astrocytes and neurons. The expression of VEGF was high in neurons and astrocytes in both the infected brain and control tissues with no difference of angiogenic activity (p = 0.40). Higher Bcl-2 expression was seen in astrocytes of infected brain tissues compared to the control tissues (p = 0.004) promoted a higher anti-apoptotic activity in astrocytes. The neurons expressed strong Bax expression in the infected brain tissues compared to the control tissues (p < 0.001), which indicated more apoptosis in neurons. Thus, neuronal death and survival of infected astrocytes together with high expression of VEGF might be associated with formation of brain tuberculosis. In conclusion, neurons could be more vulnerable than astrocytes in human tuberculosis brain with high expression of VEGF.

Keywords: Apoptosis; Astrocyte; Bcl2 and Bax; Human brain tuberculosis; Neurons; VEGF.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Astrocytes / metabolism*
  • Astrocytes / microbiology
  • Astrocytes / pathology
  • Case-Control Studies
  • Humans
  • Mycobacterium tuberculosis / pathogenicity*
  • Neurons / metabolism*
  • Neurons / microbiology
  • Neurons / pathology
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction
  • Tuberculosis, Central Nervous System / metabolism*
  • Tuberculosis, Central Nervous System / microbiology
  • Tuberculosis, Central Nervous System / pathology
  • Up-Regulation
  • Vascular Endothelial Growth Factor A / metabolism*
  • bcl-2-Associated X Protein / metabolism

Substances

  • BAX protein, human
  • BCL2 protein, human
  • Proto-Oncogene Proteins c-bcl-2
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • bcl-2-Associated X Protein