Further observations on the inhibition of tumor growth by corynebacterium parvum with cyclophosphamide.
The cytotoxic macrophage was further characterized as an important effector cell in the inhibition of tumor growth. When we administered rifampin (a semisynthetic antibiotic that interferes with macrophage function but not viability) with Corynebacterium parvum and/or cyclophosphamide to tumor-bearing C3HeB/FeJ female mice, the tumor growth-inhibitory effects of the C. parvum were reduced. Moreover, when bone marrow cells from those animals were cultured, we found a marked decrease in the cytotoxicity of macrophages comprising clonies arising from colony-forming cells (CFC) in the bone marrow. Such findings supported our contentions that 1) the cytotoxic property of macrophages originates in ancestral stem cells or CFC in bone marrow, and 2) receptor sites of the CFC (or stem cells) that respond to a stimulus for self-replication probably differ from sites that when activated produce progeny with cytotoxic properties. Although the administration of rifampin resulted in macrophages virtually devoid of cytotoxic properties, both relative and absolute numbers of CFC increased.
D000818:Animals; D003520:Cyclophosphamide / Q000378:metabolism / Q000627:therapeutic use*; D003601:Cytotoxicity Tests, Immunologic; D004347:Drug Interactions; D005260:Female; D006412:Hematopoietic Stem Cells / Q000187:drug effects / Q000276:immunology; D007167:Immunotherapy; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D008325:Mammary Neoplasms, Experimental / Q000276:immunology / Q000378:metabolism / Q000628:therapy*; D051379:Mice; D008809:Mice, Inbred C3H; D011425:Propionibacterium acnes / Q000276:immunology*; D012293:Rifampin / Q000494:pharmacology* / Q000627:therapeutic use
D003520:Cyclophosphamide; D012293:Rifampin