Fig. 6.

Protective effects of CpG-C against the deleterious effects of surgery on NK cytotoxicity, and on cytotoxicity-related NK cell markers. Mice were administered with CpG-C (100 µg/mouse, i.p.) or PBS (control) and 24 h later were further subdivided to undergo laparotomy or to serve as home cage controls. CpG-C administration resulted in a significant and marked increase in NK cytotoxicity against CT26 target cells (a), and no effects for surgery on cytotoxicity were evident in these CpG-C treated mice, despite a reduction in the number of MH-NK cells induced by surgery (NKp46 + lymphocytes) (c). In animals not treated with CpG-C, cytotoxicity levels were extremely low, probably indicating a floor effect, hindering our ability to infer about potential effects of surgery (b). The protective effects of CpG-C against the influence of surgery are also evident with respect to the percentage of MH-NK cells (NKp46 +) within the lymphocyte population (d), and the percentage of MH-NK cells expressing the murine maturation CD11b index (e) or the inhibitory NKG2A marker (f). In these three outcomes (d, e, f), CpG-C transverse the deleterious effects of surgery evident in non-CpG-C-treated animals, yielding a significant interaction between CpG-C treatment and surgery in a manner that is associated with increased NK activity