Abstract
Treatment of mouse peritoneal macrophages with IFN-γ augmented the intracellular content of S-adenosylmethionine, as measured by quantitative high-performance liquid chromatography. Accumulation of S-adenosylhomocysteine, a competitive product of S-adenosylmethionine, was not detectable, either by direct measurement of absorbance or by radioisotopic techniques in IFN-γ-treated macrophages. However, accumulation of S-adenosylhomocysteine was observed after treatment of macrophages with known inhibitors of S-adenosylhomocysteine catabolism. No inhibition of phospholipid methylation was observed upon IFN-γ treatment, indicating that no reduction of the S-adenosylmethionine to S-adenosylhomocysteine ratio is induced by IFN-γ in murine macrophages. The increased content of S-adenosylmethionine was associated with the acquisition of tumoricidal activity by macrophages upon IFN-γ treatment. LPS also augmented the cellular content of S-adenosylmethionine and activated macrophages to become cytotoxic, suggesting a common mechanism of action for IFN-γ and LPS in macrophage activation. Treatment of macrophages with cycloleucine, an agent that induces depletion of cellular S-adenosylmethionine, made the macrophages refractory to induction of cytolytic activity by IFN-γ, suggesting a critical role for S-adenosylmethionine in macrophage activation.
| Original language | English |
|---|---|
| Pages (from-to) | 2596-2604 |
| Number of pages | 9 |
| Journal | Journal of Immunology |
| Volume | 136 |
| Issue number | 7 |
| Publication status | Published - 1986 |
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Selective augmentation by recombinant interferon-γ of the intracellular content of S-adenosylmethionine in murine macrophages. / Bonvini, E.; Hoffman, T.; Herberman, R. B.; Varesio, L.
In: Journal of Immunology, Vol. 136, No. 7, 1986, p. 2596-2604.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Selective augmentation by recombinant interferon-γ of the intracellular content of S-adenosylmethionine in murine macrophages
AU - Bonvini, E.
AU - Hoffman, T.
AU - Herberman, R. B.
AU - Varesio, L.
PY - 1986
Y1 - 1986
N2 - Treatment of mouse peritoneal macrophages with IFN-γ augmented the intracellular content of S-adenosylmethionine, as measured by quantitative high-performance liquid chromatography. Accumulation of S-adenosylhomocysteine, a competitive product of S-adenosylmethionine, was not detectable, either by direct measurement of absorbance or by radioisotopic techniques in IFN-γ-treated macrophages. However, accumulation of S-adenosylhomocysteine was observed after treatment of macrophages with known inhibitors of S-adenosylhomocysteine catabolism. No inhibition of phospholipid methylation was observed upon IFN-γ treatment, indicating that no reduction of the S-adenosylmethionine to S-adenosylhomocysteine ratio is induced by IFN-γ in murine macrophages. The increased content of S-adenosylmethionine was associated with the acquisition of tumoricidal activity by macrophages upon IFN-γ treatment. LPS also augmented the cellular content of S-adenosylmethionine and activated macrophages to become cytotoxic, suggesting a common mechanism of action for IFN-γ and LPS in macrophage activation. Treatment of macrophages with cycloleucine, an agent that induces depletion of cellular S-adenosylmethionine, made the macrophages refractory to induction of cytolytic activity by IFN-γ, suggesting a critical role for S-adenosylmethionine in macrophage activation.
AB - Treatment of mouse peritoneal macrophages with IFN-γ augmented the intracellular content of S-adenosylmethionine, as measured by quantitative high-performance liquid chromatography. Accumulation of S-adenosylhomocysteine, a competitive product of S-adenosylmethionine, was not detectable, either by direct measurement of absorbance or by radioisotopic techniques in IFN-γ-treated macrophages. However, accumulation of S-adenosylhomocysteine was observed after treatment of macrophages with known inhibitors of S-adenosylhomocysteine catabolism. No inhibition of phospholipid methylation was observed upon IFN-γ treatment, indicating that no reduction of the S-adenosylmethionine to S-adenosylhomocysteine ratio is induced by IFN-γ in murine macrophages. The increased content of S-adenosylmethionine was associated with the acquisition of tumoricidal activity by macrophages upon IFN-γ treatment. LPS also augmented the cellular content of S-adenosylmethionine and activated macrophages to become cytotoxic, suggesting a common mechanism of action for IFN-γ and LPS in macrophage activation. Treatment of macrophages with cycloleucine, an agent that induces depletion of cellular S-adenosylmethionine, made the macrophages refractory to induction of cytolytic activity by IFN-γ, suggesting a critical role for S-adenosylmethionine in macrophage activation.
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M3 - Article
C2 - 3081646
AN - SCOPUS:0022654941
VL - 136
SP - 2596
EP - 2604
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 7
ER -