• T E Gardner, H Naama, and J M Daly.
• University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
• J. Surg. Res. 1995 Aug 1; 59 (2): 305-10.

AbstractIn the tumor-bearing host, depression of cell-mediated immunity has been well-demonstrated, but little is known about alterations in macrophage functions. We hypothesized that the presence of a tumor may cause functional suppression of peritoneal macrophage and splenic macrophage functions, perhaps due to prostaglandin-E2 (PGE2) and nitric oxide. C57 BL/6 mice (n = 18) were injected subcutaneously with Lewis lung carcinoma 3 tumor. Control mice (n = 18) received no tumor and were pair-fed to intake of the tumor group. On Day 21, peritoneal and splenic macrophages were harvested. Cell surface Ia expression, cytotoxicity against P815 target cells, Candida albicans killing, and production of PGE2, nitric oxide, and superoxide were measured. Mean Ia expression was decreased in tumor animals for both peritoneal and splenic macrophages. In tumor animals PGE2 production significantly increased in both peritoneal and splenic macrophages. Superoxide production significantly decreased in peritoneal macrophages but significantly increased in splenic macrophages. Nitric oxide production was also significantly depressed in tumor-bearing host peritoneal macrophages. C. albicans killing was significantly depressed in tumor animals' peritoneal macrophages but showed little change in splenic macrophages. In tumor animals cytotoxicity was significantly decreased in peritoneal macrophages but significantly increased in splenic macrophages. In the tumor-bearing host, peritoneal macrophages have significantly decreased accessory and effector functions. Splenic macrophages demonstrate decreased accessory but enhanced effector functions. PGE2, superoxide, and nitric oxide appear to be important mechanisms of altered macrophage function in the tumor-bearing host; modifying their cellular production may enhance host defense.

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