Abstract
This study examines the interaction between two types of phagocytes (P1 and P2) of the holothurian Eupentacta fraudatrix and its in vitro modulation by dexamethasone. Our results indicate that inhibition of apoptosis in P1 phagocytes by P2 phagocytes was accompanied by increased activities of antioxidant enzymes and reduced synthesis of interleukin-1α-like substances. We hypothesize that P1-phagocyte-related effects occurred in response to a high level of hydrogen peroxide produced by P2 phagocytes. The reduced anti-apoptotic effect of P2-phagocyte supernatant during prolonged incubation (24 h) was accompanied by a decline in defense reactions in P1 phagocytes due to depletion of antioxidant enzymes (catalase, glutathione reductase, and glutathione transferase). Inhibition of apoptotis in P1 phagocytes associated with upregulation of antioxidant enzyme defense in response to P2 phagocytes preincubated with dexamethasone (100 µM) indicates that P2 phagocytes affect P1 phagocytes via a ROS-associated mechanism. Thus, our data provide evidence that P1 and P2 phagocytes exhibit their maximum activity at different stages of the immune response, thus causing inhibition of activity in target cells during prolonged exposure. Dexamethasone enhances these effects.
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