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Differential expression of NF-kappaB in mycobacteria infected THP-1 affects apoptosis

Rohan Dhiman1, Manoj Raje, Sekhar Majumdar

  • 1Division of Cell Biology and Immunology, Institute of Microbial Technology (CSIR), Chandigarh 160 036, India.

Biochimica Et Biophysica Acta
|January 6, 2007
PubMed

Insights

Nuclear Factor-kappa B (NF-kappaB) plays a key role in tuberculosis infection. Inhibiting NF-kappaB in THP-1 cells increased apoptosis and reduced mycobacterial growth, suggesting its importance in virulent Mycobacterium tuberculosis survival.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Tuberculosis remains a significant global health challenge.
  • Understanding host-pathogen interactions is crucial for developing effective treatments.
  • Nuclear Factor-kappa B (NF-kappaB) is a key transcription factor involved in immune responses.

Purpose of the Study:

  • To investigate the role of NF-kappaB in the infection of THP-1 cells by virulent (Mycobacterium tuberculosis H37Rv) and avirulent (M. tuberculosis H37Ra) strains.
  • To determine how NF-kappaB inactivation affects host cell apoptosis and intracellular mycobacterial growth.

Main Methods:

  • Generated a THP-1 cell line with inactivated NF-kappaB using pCMV-IkappaBalphaM dn.
  • Infected these cells with M. tuberculosis H37Rv and M. tuberculosis H37Ra.
  • Assessed apoptosis, mitochondrial membrane potential, cytochrome c release, caspase-3 activation, TNF-alpha production, and intracellular bacterial growth.

Main Results:

  • NF-kappaB inactivation led to increased apoptosis in infected THP-1 cells.
  • Inhibition of NF-kappaB decreased mitochondrial membrane potential, increased cytochrome c release, activated caspase-3, and enhanced TNF-alpha production.
  • NF-kappaB inactivation inhibited intracellular mycobacterial growth.
  • Virulent M. tuberculosis H37Rv differentially activated NF-kappaB compared to the avirulent strain, up-regulating the anti-apoptotic factor bfl-1/A1.

Conclusions:

  • NF-kappaB activation is critical for the survival and virulence of Mycobacterium tuberculosis within macrophages.
  • Targeting NF-kappaB signaling presents a potential therapeutic strategy against tuberculosis.

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