Androgens and the immunocompetence handicap hypothesis: Unraveling direct and indirect pathways of immunosuppression in song sparrows
Author
Summary, in English
The immunocompetence handicap hypothesis proposes that testosterone (T)-dependent sexual signals are honest indicators of male health or genetic quality because only high-quality males are able to withstand the obligate effects of T-induced immunosuppression. In birds, the basic assumption that T suppresses immune function is equivocal, and the physiological mechanisms underlying T-induced immunosuppression remain to be investigated. We explored the proximate pathways of T-induced immunosuppression in song sparrows (Melospiza melodia) by treating captive nonbreeding males with different androgens and measuring several components of acquired immune function. Males implanted with T suppressed cell-mediated and humoral immune responses compared to males implanted with 5proportional to-dihydrotestosterone (DHT), dehydroepiandrosterone, or control ( empty) implants. Furthermore, T treatment increased plasma levels of corticosterone and decreased body mass and fat stores in relation to other treatments. The failure of DHT to depress immune function suggests that T-induced immunosuppression does not occur through a direct pathway because both T and DHT bind to androgen receptors on target cells. Instead, we outline indirect pathways that are likely responsible for suppression of the avian immune system that include stress-induced immunosuppression, aromatization to estrogen, and alterations in energy allocation that constrain expenditures toward immune system activation.
Department/s
Publishing year
2004
Language
English
Pages
490-505
Publication/Series
American Naturalist
Volume
164
Issue
4
Full text
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Links
Document type
Journal article review
Publisher
University of Chicago Press
Topic
- Biological Sciences
Keywords
- immunosuppression
- song sparrow
- testosterone
- corticosterone
- androgens
- immunocompetence
Status
Published
Research group
- Molecular Ecology and Evolution Lab
ISBN/ISSN/Other
- ISSN: 0003-0147