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Hassan A. Naama, FRCS; Vivian E. Mack, MD; Gordon P. Smyth, MB,BCh; Philip P. Stapleton, PhD; John M. Daly, MD

Arch Surg. 2001;136:804-809.

Background  The tumor-bearing state is known to induce immune dysfunction that contributes to increased infectious complications and tumor progression. However, the mechanisms underlying this immunosuppression remain unclear.

Hypothesis  Macrophage (MO) dysfunction may play a role in tumor-induced immunosuppression.

Design and Main Outcome Measures  Using a murine model, this study investigated the effects of melanoma growth on peritoneal macrophage effector molecule and prostaglandin production, MO-mediated cytotoxicity, and candidacidal mechanisms. Female C57BL/6 mice were inoculated with 106 B16 melanoma cells or a salt solution subcutaneously. Mice were euthanized 3 weeks later and peritoneal MOs were harvested and assayed for nitric oxide, superoxide anion, tumor necrosis factor , and prostaglandin E₂production. Macrophage-mediated cytotoxicity against B16 melanoma targets and MO candidacidal mechanisms were also measured.

Results  Macrophage production of nitric oxide, superoxide anion, and tumor necrosis factor were significantly decreased, while prostaglandin E₂production was increased in MOs from melanoma-bearing mice. Concomitantly, MO-mediated cytotoxicity and candidacidal mechanisms were significantly impaired.

Conclusions  Melanoma growth leads to decreased MO effector molecule production, increased prostaglandin E₂production, and impaired MO cytotoxic and candidacidal mechanisms. These results may help explain the observed increased infectious complications in the tumor-bearing host. Strategies aimed at restoring MO function may have therapeutic potential.

From the Departments of Surgery, Weill Medical College of Cornell University (Drs Naama, Mack, Smyth, Stapleton, and Daly); and The New York Presbyterian Hospital (Drs Naama, Mack, and Daly), New York City.

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