OWEN-ASHLEY, N. T.*; HASSELQUIST, D.; WINGFIELD, J. C.; Univ. of Washington, Seattle; Lund University, Sweden; Univ. of Washington, Seattle: Examining the indirect pathways of testosterone-induced immunosuppression in male songbirds. I.) Effects of corticosterone and estradiol on acquired immune function

Recent evidence suggests that testosterone (T)-induced immunosuppression in male birds occurs through a combination of indirect pathways rather than through direct activation of androgen receptors on immune cells. It is hypothesized that other steroids, such as glucocorticosteroids and estrogens, contribute indirectly to T-induced immunosuppression, as both steroids have immunomodulatory properties, and they can increase in the circulation (corticosterone via binding globulins) or within immune cells (estradiol via aromatization) as a result of T implantation. We examined if these steroids suppressed acquired immune function in male nonbreeding song sparrows (Melospiza melodia). As predicted, cell-mediated immune responses to phytohemagglutinin (PHA) were reduced in birds implanted with corticosterone relative to blank-implanted controls. In a separate experiment, estradiol implants in males suppressed both cell-mediated responses to PHA and primary and secondary humoral responses to a novel antigen, keyhole limpet hemocyanin (KLH), compared to controls. However, baseline corticosterone levels were elevated in estradiol-implanted males relative to controls, indicating that suppression of the immune system could be mediated through stress-induced mechanisms rather than through activation of estrogen receptors. These results provide additional evidence that other endocrine pathways could be responsible for suppression of immune function instead of T. Further experiments using aromatase inhibitors are needed to clarify if estrogen indirectly regulates T-induced immunosuppression in male songbirds.