title: Effects of corticosterone on innate and humoral immune functions and oxidative stress in barn owl nestlings.
abstract: The costs of coping with stressful situations are traded-off against other functions such as immune responses. This trade-off may explain why corticosterone secretion reduces immune reactions. Corticosterone differentially affects various immunity components. However, which component is suppressed varies between studies. It remains unclear whether the trade-off in energy, nutrition, autoimmunity or oxidative stress accounts for differential immunosuppression. In this study, we investigated whether corticosterone differentially affects the constitutive innate and humoral acquired immunity. We used barn owl nestlings, implanting 50% with a corticosterone-releasing pellet and the other 50% with a placebo pellet. To measure the effect on humoral immunity we vaccinated 50% of the corticosterone-nestlings and 50% of the placebo-nestlings with the antigens 'Tetravac' and the other 50% were injected with PBS. To assess the costs of elevated corticosterone, we measured body mass and resistance to oxidative stress. Administration of corticosterone increased corticosterone levels whereas vaccination induced the production of antibodies. Corticosterone reduced the production of antibodies, but it did not significantly affect the constitutive innate immunity. Corticosterone reduced body growth and resistance to oxidative stress. Under stressful conditions barn owl nestlings seem to keep the constitutive innate immunity, whereas elevated corticosterone levels negatively affected inducible immune responses. We found evidence that mounting a humoral immune reaction is not costly in terms of growth, but reduces the resistance to oxidative stress independently of corticosterone administration. We suggest that humoral immunity is suppressed because the risk of immunopathologies may be disproportionately high when mounting an antibody response under stressful situations.
authors.affiliation: Swiss Ornithological Institute, CH-6204 Sempach, Switzerland. kimstier@yahoo.de
authors.forename: Kim Silvana
authors.initials: KS
authors.lastname: Stier
authors.forename: Bettina
authors.initials: B
authors.lastname: Almasi
authors.forename: Julien
authors.initials: J
authors.lastname: Gasparini
authors.forename: Romain
authors.initials: R
authors.lastname: Piault
authors.forename: Alexandre
authors.initials: A
authors.lastname: Roulin
authors.forename: Lukas
authors.initials: L
authors.lastname: Jenni
mesh_terms: D000818:Animals; D000917:Antibody Formation / Q000187:drug effects*; D049628:Body Size; D003345:Corticosterone / Q000097:blood / Q000494:pharmacology*; D007113:Immunity, Innate / Q000187:drug effects*; D018384:Oxidative Stress; D020305:Strigiformes / Q000254:growth & development / Q000276:immunology* / Q000502:physiology
chemical_list: D003345:Corticosterone