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Tumor necrosis factor alpha acts as an autocrine second signal with gamma interferon to induce nitric oxide in group

K J Goodrum1, J Dierksheide, B J Yoder

  • 1Department of Biological Sciences, Ohio University, Athens 45701-2979, USA.

Infection and Immunity
|September 1, 1995
PubMed

Insights

Tumor necrosis factor alpha mediates nitric oxide production in macrophages stimulated by group B streptococci and interferon. Inhibiting this cytokine or phagocytosis blocks nitric oxide generation.

Area of Science:

  • Immunology
  • Microbiology
  • Cellular Biology

Background:

  • Macrophages play a crucial role in innate immunity, producing nitric oxide (NO) to combat pathogens.
  • Group B Streptococcus (GBS) is a significant human pathogen, particularly in neonates.
  • Interferon-gamma (IFN-γ) is a key cytokine that activates macrophages for antimicrobial functions.

Purpose of the Study:

  • To investigate the role of tumor necrosis factor alpha (TNF-α) in GBS-induced nitric oxide production by macrophages.
  • To elucidate the signaling pathway linking GBS phagocytosis to NO synthesis in IFN-γ-primed macrophages.

Main Methods:

  • Primary mouse macrophages were treated with GBS and IFN-γ.
  • Nitric oxide production was measured.
  • Inhibitors of phagocytosis (cytochalasin B) and TNF-α neutralization antibodies were employed.

Main Results:

  • Nitric oxide production was significantly inhibited by cytochalasin B, indicating a role for phagocytosis.
  • Antibody-mediated neutralization of macrophage-derived TNF-α also inhibited nitric oxide production.
  • These findings demonstrate that phagocytosis-induced TNF-α is essential for GBS-stimulated NO production in IFN-γ-treated macrophages.

Conclusions:

  • Macrophage-derived TNF-α is a critical mediator of nitric oxide production in response to GBS infection.
  • The study highlights a specific molecular mechanism by which macrophages control bacterial infections via NO and TNF-α signaling.

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