Defective production of reactive oxygen intermediates by tumor-associated macrophages exposed to phorbol ester.
Macrophages were isolated from poorly immunogenic metastatic sarcomas (mFS6 and MN/MCA1) of C57BL/6 origin. Tumor-associated macrophages (TAM) showed little release of superoxide when exposed to phorbol myristate acetate. When exposed to a phagocytic stimulus (zymosan), TAM released appreciable amounts of superoxide. TAM had a lower number of specific binding sites for phorbol esters than resident or caseinate-elicited peritoneal macrophages, but had normal NADPH-cytochrome C reductase. The tumor environment, possibly through previously demonstrated products of neoplastic cells, may influence the functional status of in situ macrophages and, thus, impair host anti-tumor and anti-microbial defense mechanisms.
D000818:Animals; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009251:NADPH-Ferrihemoprotein Reductase / Q000378:metabolism; D015240:Phorbol 12,13-Dibutyrate; D010703:Phorbol Esters / Q000378:metabolism; D012513:Sarcoma, Experimental / Q000473:pathology*; D013481:Superoxides / Q000378:metabolism*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*; D015054:Zymosan / Q000494:pharmacology
D010703:Phorbol Esters; D013481:Superoxides; D015240:Phorbol 12,13-Dibutyrate; D015054:Zymosan; D009251:NADPH-Ferrihemoprotein Reductase; D013755:Tetradecanoylphorbol Acetate