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Macrophages release tumor necrosis factor alpha and interleukin-12 in response to intracellular Bacillus anthracis

Alison K Pickering1, Tod J Merkel

  • 1Laboratory of Respiratory and Special Pathogens, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA.

Infection and Immunity
|April 23, 2004
PubMed

Insights

Bacillus anthracis infection stimulates macrophages to produce tumor necrosis factor alpha and interleukin-12 (IL-12). Macrophages release more IL-12 when exposed to B. anthracis spores and lipopolysaccharide, with no observed inhibition of cytokine responses.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Macrophages are key immune cells involved in host defense against bacterial pathogens.
  • Bacillus anthracis is a dangerous bacterium that causes anthrax.
  • Cytokine production by macrophages is critical for regulating immune responses.

Purpose of the Study:

  • To investigate the cytokine response of murine macrophages upon infection with Bacillus anthracis.
  • To determine the effect of B. anthracis spores and lipopolysaccharide on macrophage cytokine production.

Main Methods:

  • Infection of a murine macrophage cell line with Bacillus anthracis.
  • Stimulation of macrophages with B. anthracis spores in combination with lipopolysaccharide.
  • Measurement of cytokine production, including tumor necrosis factor alpha and interleukin-12 (IL-12).

Main Results:

  • Bacillus anthracis infection induced the production of tumor necrosis factor alpha and IL-12 in macrophages.
  • Co-exposure to B. anthracis spores and lipopolysaccharide led to increased IL-12 release.
  • No evidence of suppressed cytokine responses was observed in infected macrophages.

Conclusions:

  • Murine macrophages mount a pro-inflammatory cytokine response upon B. anthracis infection.
  • The combination of B. anthracis spores and lipopolysaccharide enhances IL-12 production.
  • B. anthracis infection does not inhibit the macrophage's ability to produce key cytokines.

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