Stress and immunological phagocytosis: possible nongenomic action of corticosterone

Some immunological responses triggered by stress can be mediated by corticosterone activity through cytosolic receptors regulating gene expression. There are, however some reports on the possibility of a nongenomic effect of this hormone to explain phenomena observed in a few minutes. We have found that macrophages from mice subjected to 10 min of cold stress (at -15 degrees C) showed a lower phagocytic capacity mediated by Fcgamma-receptors than cells from control animals. Treating mice with glucocorticoid antagonist RU 486 did not block the decrease in phagocytic capacity. This inhibitory effect on phagocytosis was also observed by experiments in vitro with corticosterone in the concentration found in serum after stress, and could not be prevented by RU 486, actinomicyn D or cycloheximide. These results indicate that corticosterone could affect phagocytosis by macrophages through a nongenomic mechanism, and may have physiological implications.