Meeting Abstract
The activation of the stress response can affect immune function in many species of free-living birds. It is unclear, however, if the direction of these effects depend on the duration of the stressor, how the stress response regulates immune function, and which components of the immune system are altered. We used adult male House Sparrows (Passer domesticus) to address these uncertainties. Specifically, we investigated 1) the interaction between an activated stress response and the innate immune response and 2) the possible roles of the stress hormone, corticosterone (CORT), over this interaction. We focused on the innate immune system because it is the first line of defense against pathogens. The stress response was induced by restraining birds for 10 minutes or 2 hours. The strength of the innate immune response was measured by how well its plasma components could recognize and lyse foreign cells (agglutination-lysis assay) and kill bacteria (bacterial killing assay). Innate immune measures were reduced by 10 minutes and remained low for 2 hours after the activation of the stress response. When birds were treated with mitotane to inhibit stress-induced (SI) elevation of plasma CORT, SI immunosuppression did not occur. In fact, mitotane-treated birds showed enhanced bacterial killing capacity relative to control birds. When birds were treated with RU486 to antagonize the glucocorticoid receptor, activation of the stress response did not decrease agglutination scores but still reduced bacterial killing capacity. These results suggest that SI levels of plasma CORT regulate the suppression of the innate immune response during the stress response, and that this regulation may be partially mediated through the glucocorticoid receptor. These studies were funded by CAP LTER, ASU Sigma Xi, and NSF IOB 1026620 to PD.
