Relationship of the suppression of macrophage mediated tumor cytotoxicity in conjunction with secretion of prostaglandin from the macrophages of breast cancer patients.
Peripheral blood monocyte derived macrophages obtained from breast cancer patients are non-cytotoxic towards human tumor cells. However, when indomethacin, a prostaglandin synthetase inhibitor, was added to the macrophage tumor cell incubation mixture, the breast cancer patient's macrophages became capable of killing the tumor cells. Furthermore, the macrophage preparations obtained from breast cancer patients demonstrated a 64% increase in the secretion of PGE2, when compared with macrophages obtained from normal donors. It is already known that prostaglandin can inhibit both natural lymphocyte cytotoxicity and antibody dependent cell-mediated cytotoxicity against human tumor cells in vitro. These results indicate that increased synthesis of prostaglandin can also inhibit macrophage mediated cytotoxicity. Therefore, it is possible that manipulation of this mechanism might enhance the effectiveness of the macrophage response and should be a consideration in assessing macrophage-tumor cell interaction in vitro and in vivo.
D001943:Breast Neoplasms / Q000276:immunology* / Q000378:metabolism; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D005260:Female; D006801:Humans; D007165:Immunosuppression Therapy; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism*; D014361:Trypsin Inhibitors / Q000494:pharmacology
D008070:Lipopolysaccharides; D011453:Prostaglandins; D014361:Trypsin Inhibitors; D007213:Indomethacin