TY - JOUR
T1 - Macrophage-activating factor extracted from mycoplasmas
AU - Takema, Morio
AU - Oka, Shogo
AU - Uno, Kazuko
AU - Nakamura, Shinji
AU - Arita, Hitoshi
AU - Tawara, Katsuya
AU - Inaba, Kayo
AU - Muramatsu, Shigeru
PY - 1991/1
Y1 - 1991/1
N2 - Mycoplasmas (M. gallisepticum, chicken mycoplasmas), in concert with interferon γ (IFNγ), were effective in activating macrophages (Mθ) to be tumoricidal. The Mθ-activating capacity of mycoplasmas was maintained after treatment with heat, 0.1 M NaOH, 1 M HC1, or trypsin. Mθ-activating factor was extracted from mycoplasmas with chloroform/methanol and water (Mf-B). Mf-B was also effective in activating Mθ in the presence of IFNγ. The threshold dose of Mf-B for Mθ of ordinary C3H/He mice and that for those of C3H/HeJ mice, the latter being known to be low responders to bacterial lipopolysaccharide, were actually the same. This seems to indicate that the effectiveness of Mf-B was not attributable to possibly contaminating lipopolysaccharides, and that the pathway of activity of Mf-B is different from that of lipopolysaccharides. Since the Mθ-activating principle was only a very small part of Mf-B, we have not yet succeeded in identifying it, but there was no evidence that it was protein, nucleic acid, sugar, or lipid. The cytotoxicity of Mθ activated by Mf-B plus IFNγ was dependent on l-arginine in the culture, suggesting that arginine metabolites are involved in Mθ cytotoxicity. Mf-B induced a small amount of tumor necrosis factor in Mθ, and this induction was markedly enhanced by IFNγ.
AB - Mycoplasmas (M. gallisepticum, chicken mycoplasmas), in concert with interferon γ (IFNγ), were effective in activating macrophages (Mθ) to be tumoricidal. The Mθ-activating capacity of mycoplasmas was maintained after treatment with heat, 0.1 M NaOH, 1 M HC1, or trypsin. Mθ-activating factor was extracted from mycoplasmas with chloroform/methanol and water (Mf-B). Mf-B was also effective in activating Mθ in the presence of IFNγ. The threshold dose of Mf-B for Mθ of ordinary C3H/He mice and that for those of C3H/HeJ mice, the latter being known to be low responders to bacterial lipopolysaccharide, were actually the same. This seems to indicate that the effectiveness of Mf-B was not attributable to possibly contaminating lipopolysaccharides, and that the pathway of activity of Mf-B is different from that of lipopolysaccharides. Since the Mθ-activating principle was only a very small part of Mf-B, we have not yet succeeded in identifying it, but there was no evidence that it was protein, nucleic acid, sugar, or lipid. The cytotoxicity of Mθ activated by Mf-B plus IFNγ was dependent on l-arginine in the culture, suggesting that arginine metabolites are involved in Mθ cytotoxicity. Mf-B induced a small amount of tumor necrosis factor in Mθ, and this induction was markedly enhanced by IFNγ.
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U2 - 10.1007/BF01742526
DO - 10.1007/BF01742526
M3 - Article
C2 - 1902396
AN - SCOPUS:0026036464
SN - 0340-7004
VL - 33
SP - 39
EP - 44
JO - Cancer Immunology Immunotherapy
JF - Cancer Immunology Immunotherapy
IS - 1
ER -