Tumor necrosis factor alpha acts as an autocrine second signal with gamma interferon to induce nitric oxide in group B streptococcus-treated macrophages.
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.
Goodrum
K J
KJ
Department of Biological Sciences, Ohio University, Athens 45701-2979, USA.
Dierksheide
J
J
Yoder
B J
BJ
D000818:Animals; D002478:Cells, Cultured; D003571:Cytochalasin B / Q000494:pharmacology; D007371:Interferon-gamma / Q000494:pharmacology*; D008264:Macrophages / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D009569:Nitric Oxide / Q000502:physiology*; D010587:Phagocytosis; D011994:Recombinant Proteins; D013292:Streptococcus agalactiae / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D003571:Cytochalasin B; D007371:Interferon-gamma