Mechanism of production of interferon-gamma: role of arachidonic acid metabolites

G. Antonelli, A. Mastino, P. Amicucci, O. Turriziani, C. Favalli, E. Garaci

Research output: Contribution to journalArticlepeer-review


The effects of arachidonic acid metabolites on mitogen-induced interferon (IFN)-gamma production by human peripheral blood mononuclear cells (PBMC) were examined. Both prostaglandins E2 (PGE2) and leukotrienes B4 (LTB4) were produced after macrophage activation stimulated by galactose oxidase (GO) and Staphylococcal enterotoxin B (SEB), two well known inducers of IFN-gamma. To test the involvement of PGE2 and LTB4 in IFN-gamma production, GO- and SEB-activated PBMC were treated with two inhibitors of cycloxygenase (aspirin and indomethacin) and with an inhibitor of lipoxygenase [nordihydroguaiaretic acid (NDGA)]. The results of these experiments showed that aspirin and indomethacin cause a marked increase of IFN-gamma production by GO- and SEB-activated PBMC. On the contrary, NDGA treatment reduced IFN-gamma production induced by the same agents. Moreover, whereas the addition of exegenous PGE2 reduces IFN gamma-production, the addition of exogenous LTB4 does not affect IFN-gamma production. Taken together these findings indicate that arachidonic acid metabolites, produced during mitogenic activation, are involved in the regulation of IFN-gamma production and suggest that, in our system, LTB4 exerts a positive modulating signal while PGE2 represents a negative signal.

Original languageEnglish
Pages (from-to)13-18
Number of pages6
JournalJournal of Biological Regulators and Homeostatic Agents
Issue number1
Publication statusPublished - 1990

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Endocrinology
  • Physiology
  • Immunology
  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Physiology (medical)


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