Inhibition of lung colonization of mouse colon 26 adenocarcinoma by recombinant mouse interferon beta through a modification of platelet function

Recombinant murine interferon beta (MuIFN-beta) given i.v. efficiently inhibited both pulmonary arrest and formation of lung colonies of NL-17, a highly metastatic variant of mouse colon adenocarcinoma 26. NL-17 was rather resistant to MuIFN-beta in vitro and was highly resistant to natural killer cells of mice even though they were treated in vivo with MuIFN-beta. Platelets isolated from MuIFN-beta-treated mice showed reduced aggregating activity induced by NL-17. Since lung colonization by NL-17 is influenced by platelet aggregation, the inhibition of colonization by MuIFN-beta could be partly mediated through modification of platelet function in vivo. The effect of MuIFN-beta on platelet function and its subsequent inhibition of lung colony formation give new insights into the action of recombinant MuIFN-beta.