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In staphylococcal infection the changes in functional ability of macrophages occur: their oxygen-depending bactericidity and adenosine-desaminase activity are depressed 5-nucleotidase ability increases. Introduction of homologous alpha-IFN in the dose of 1 x 10(3) u/mouse leads to enhancing macrophage bactericidity of the animals infected, inhibits their 5-nucleotidase activity and enhances adenosine desaminase one. Influence of alpha-IFN on the activity of adenosine metabolism enzymes in macrophages can be considered one of the most important mechanisms of its modulating effect in bacterial infections.

It has been established that the administration of homologous interferon to mice activates the production by splenocytes of a factor increasing the bactericidal properties of macrophages in the peritoneal exudate. The activation effect was dose-dependent. The maximum production was noted on day 3 after the injection of interferon, type I, or its inducers. Cell-producers of the factor are mainly lymphocytes.

The effect of the in vivo treatment with synthetic interferon inducer B-58 on natural killer (NK) and cytostatic cell activity was studied in CBA and A/Sn mice. A marked increase in NK cell activity against target cells YAC-1 was observed in the spleen of CBA mice within 4 days after treatment. On the other hand, NK activity in A/Sn mice was not affected by B-58. However, B-58 was shown to enhance cytostatic cell activity both in CBA and A/Sn mice, when tested against target cells P 815.