Abstract
Previous work has demonstrated that cell-mediated immune function in rats is better preserved after laparoscopic than open surgery. We have also shown that tumors are more easily established in mice and grow larger after sham laparotomy than after pneumoperitoneum. The purpose of this study is to determine if the functional status of the cell-mediated immune system influences postoperative tumor growth. Immunocompetent (study 1) and T-cell deficient athymic (study 2) mice were injected with mouse mammary carcinoma cells in the dorsal skin. Mice then underwent either no procedure, midline laparotomy, or carbon dioxide pneumoperitoneum. Tumor masses on postoperative day 12 were compared. In immunocompetent mice, laparotomy group tumors were nearly twice as large as laparoscopy group tumors (p < 0.02), which were 1.5 times as large as control group tumors (NS). In the athymic model, however, differences between the sham laparotomy and pneumoperitoneum groups were lost (p > 0.5). Tumors grew much larger in the athymic control mice than in the immunocompetent control mice (p < 0.01). We conclude that T-cell function plays a significant role in host containment of mouse mammary carcinoma and in the mechanism of differences in tumor growth observed after laparotomy and pneumoperitoneum.
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