Hyperthermic Modulation of Respiratory Inhibition Factor- and Iron Releasing Factor-dependent Macrophage Murine Tumor Cytotoxicity

摘要: Hyperthermia modulated the cytotoxic activities of murine macrophages cocultured with EMT-6 tumor cells, altered production monokines RIF (respiratory inhibition factor) and FeRF (iron-releasing by these effector perturbed against cells. Cytotoxic heated activated Bacillus Calmette-Guerin were inhibited heat doses 40.5 degrees C for greater than or equal to 1 h if heating preceded triggering endotoxin lipopolysaccharide; however, better retained 2 h. Treatment-sequence dependencies also found in secretion some that participate macrophage effects. Secretion both was slightly augmented at least occurred several hours before 40.5-43 24 39-40.5 C. If nearly simultaneous it hours, there a dose-dependent decrease monokine secretion. The sensitivity cell targets modified treatment sequence. When cells treated RIF- FeRF-containing conditioned supernatants C, RIF-treated became sensitized FeRF-treated response had been after heating. Chronic showed less dependence on Similar observations have recently made our laboratory interaction necrosis factor pathways hyperthermia (Klostergaard et al., J. Biol. Response Modif., press, 1989; Tomasovic Int. Hyperthermia, 1989). Those results present support hypothesis actions cytotoxicity endogenously added can be appropriately constructed sequences combining either priming/triggering