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Tumour necrosis factor alpha mediated apoptosis in murine macrophages by Salmonella enterica serovar Typhi under

Vishal Chanana1, Siddharth Majumdar, Praveen Rishi

  • 1Department of Microbiology, Panjab University, Chandigarh, India.

FEMS Immunology and Medical Microbiology
|July 13, 2006
PubMed

Insights

Oxidative stressed Salmonella enterica serovar Typhi significantly increases macrophage apoptosis compared to normal conditions. This suggests a mechanism for Salmonella evasion of the immune system, impacting host-pathogen interactions.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogen-host interactions

Background:

  • Invasive Salmonella can induce macrophage apoptosis to evade innate immunity.
  • The role of oxidative stress in Salmonella-induced apoptosis is not fully understood.
  • Understanding these mechanisms is crucial for developing effective interventions.

Purpose of the Study:

  • To investigate the effect of oxidative stress on Salmonella enterica serovar Typhi's ability to induce macrophage apoptosis.
  • To explore the molecular mechanisms underlying this process.

Main Methods:

  • Salmonella enterica serovar Typhi was cultured under hydrogen peroxide-induced oxidative stress.
  • Murine macrophages were exposed to both stressed and non-stressed Salmonella.
  • Apoptosis levels, oxidant/antioxidant levels, and cytokine production were measured.

Main Results:

  • Oxidative stressed Salmonella induced apoptosis in 51% of macrophages, versus 32% for non-stressed Salmonella.
  • Increased oxidants and decreased antioxidants correlated with elevated levels of tumor necrosis factor alpha, interleukin-1alpha, and interleukin-6.
  • These changes suggest a role for lipid peroxidation and superoxide dismutase in cytokine-mediated apoptosis.

Conclusions:

  • Oxidative stress enhances Salmonella's ability to induce macrophage apoptosis.
  • Tumor necrosis factor alpha and other cytokines may mediate this apoptosis via lipid peroxidation and superoxide dismutase.
  • Findings offer insights into host-pathogen interactions and potential therapeutic targets.

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