Abstract
Stress-induced inhibition of innate immune activity is widespread in free-ranging birds, but the mechanisms that are responsible for this inhibition are poorly understood. We previously demonstrated that an increase in plasma corticosterone (CORT), the primary avian glucocorticoid, is necessary for the inhibition of natural antibody- and complement-mediated as well as bactericidal activities to occur during stress. Here we investigated the role of glucocorticoid receptors in stress-induced inhibition of natural antibody- and complement-mediated activities and bactericidal activity within non-genomic (<10 min) and genomic (<120 min) time frames in male House Sparrows, Passer domesticus. Treatment with the selective glucocorticoid receptor antagonist mifepristone (RU486) attenuated stress-induced suppression of natural antibody-mediated activity within 10 min and 120 min of experimental stress. By contrast, this treatment did not influence stress-induced suppression of complement-mediated or bactericidal activity. These results suggest that stress-induced elevated plasma CORT inhibits natural antibody-mediated activity, but not complement-mediated or bactericidal activity, by activating glucocorticoid receptors, and that both non-genomic and genomic mechanisms underlie this activation. Additional research is needed to identify the receptors that regulate inhibitory effects of elevated plasma CORT on complement-mediated and bactericidal activity.