Tumor necrosis factor alpha acts as an autocrine second signal with gamma interferon to induce nitric oxide in group B streptococcus-treated macrophages

Infect Immun. 1995 Sep;63(9):3715-7. doi: 10.1128/iai.63.9.3715-3717.1995.

Abstract

Nitric oxide production by mouse macrophages treated with group B streptococci and gamma interferon was inhibited by cytochalasin B or by antibody neutralization of macrophage-derived tumor necrosis factor alpha. Phagocytosis-induced tumor necrosis factor alpha is responsible for group B streptococcus-induced nitric oxide production in interferon-treated macrophages.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Cytochalasin B / pharmacology
  • Interferon-gamma / pharmacology*
  • Macrophages / metabolism*
  • Mice
  • Mice, Inbred BALB C
  • Nitric Oxide / physiology*
  • Phagocytosis
  • Recombinant Proteins
  • Streptococcus agalactiae / physiology*
  • Tumor Necrosis Factor-alpha / physiology*

Substances

  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Cytochalasin B
  • Interferon-gamma