INHIBITORY EFFECT OF MURINE RECOMBINANT INTERFERON-(BETA) ON THE PULMONARY METASTASIS OF B-16 MELANOMA

  • 1 August 1986
    • journal article
    • research article
    • Vol. 77  (8) , 774-781
Abstract
The antitumor effect of murine recombinant interferon (.beta.) [Mu-rIFN(.beta.)] was examined on artificial metastasis of B-16 melanoma in C57BL/6 mice. The numbers of pulmonary nodules were significantly decreased to 16.7 .+-. 4.7 (P < 0.01), 9.5 .+-. 4.2 (P < 0.01), 7.1 .+-. 5.6 (P < 0.01) in mice given 20,000 units of Mu-rIFN(.beta.) intraperitoneally (ip) 24, 6, and 3 hr before intravenous tumor inoculation, respectively, compared with the control group of mice (57.1 .+-. 1.4), if B-16 melanoma cells (5 .times. 105) were intravenously injected 28 days before the experiment. In mice given 20,000 units of Mu-rIFN (.beta.) ip 24, 6, and 3 hr before the experiment, the natural killer (NK) activities of spleen cells against YAC-1 cells were elevated to 45.5 .+-. 6.1% 53.7 .+-. 3.4%, 43.2 .+-. 6.5%, respectively, compared with NK activities in control mice (20.3 .+-. 3.1%). Similarly, NK activities against B-16 melonama cells were also elevated in mice given Mu-rIFN(.beta.). Pretreatment with anti-asialo GM1 antibody and carrageenan reduced the inhibitory effect of Mu-rIFN(.beta.) on the pulmonary metastasis. In vitro colony inhibition of more than 50% was not observed even if B-16 melanoma cells were incubated with 100,000 units/ml of Mu-rIFN(.beta.). From these results, it can be concluded that the inhibition of pulmonary metastasis by Mu-rIFN(.beta.) is mediated via host defense mechanisms and that NK cells and macrophages are both important for the inhibition.