Enzymically-modified human mammary carcinoma cells: modulators of macrophage functions

Human mammary carcinoma cells (HMCC), vibrio cholera neuraminidase (VCN) treated HMCC(VCN-HMCC); glutaraldehyde fixed VCN-HMCC(Glut-VCN-HMCC), normal mammary epithelial cells (HMEC), VCN treated HNEC (VCN-HNEC) and glutaraldehyde fixed VCN-HNEC (Glut-VCN HNEC) were prepared and injected into separate groups of mice. Intraperitoneal injection of phytohemagglutinin (PHA) produced a delayed type of inflammatory reaction characterized by an accumulation of macrophages. Injection of HNEC, VCN-HNEC, and Glut-VCN-HNEC had no effect, HMCC inhibited, and VCN-HMCC and Glut-VCN-HMCC increased both the number and the tumoricidal activity of peritoneal macrophages. Cell-free media (CFM) harvested from cultures of HMCC alone or mixed with lymphocytes from patients with mammary carcinoma inhibited, whereas CFM from mixed cultures of HMCC and lymphocytes from normal subjects had no effect on, the chemotactic response and migration of normal peritoneal macrophages. CFM was passes through a series of Amicon membranes, the active principle passed through membrane PM-10 but was retained by PM-5 suggesting a molecular weight of less than 10,000. In culture, HNEC, VCN-HNEC and VCN-HMCC proliferated as sheets of single cell monolayers, whereas HMCC began to spread as a monolayer, but as cellular density increased it formed cell foci, cell colonies and cell clusters packed into solid tissuelike masses.