Mouse peritoneal macrophages (MΦ) expressed enhanced tumoricidal activity upon in vitro stimulation either with the lymphokine MΦ-activating factor (MAF) or with fibroblast interferon (IFN-β). In contrast, MΦ suppressive activity on lymphoproliferation was not affected by MAF pretreatment, but was drastically reduced or abolished by IFN-β. Catalase, the enzyme involved in the destruction of hydrogen peroxide (H2O2), did significantly decrease MΦ suppressive capacity but had no effect on MΦ tumoricidal activity. Analysis of the phagocytosis-dependent H2O2 production by IFN-β-treated MΦ demonstrated a strong impairment of the oxygen metabolite release, which strictly paralleled the decreased MΦ suppressive capacity. On the other hand, MAF did not modify H2O2 release by MΦ. Studies on MΦ antibacterial activity against Salmonella typhimurium, a function thought to depend upon H2O2 production, showed that exposure of MΦ to IFN-β significantly impaired their bactericidal and bacteriostatic capacity, again in close correlation with the decrease in H2O2 production. Thus, IFN-β appears as modulating both suppressive and antibacterial capacities of MΦ through reduction of their oxygen metabolism, whereas regulation of MΦ anti-tumour activity is possibly controlled by different mechanisms.
|Number of pages||10|
|Publication status||Published - 1983|
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