INVESTIGADORES
MARIN Raul Hector
artículos
Título:
The effects of testosterone on immune function in quail selected for
Autor/es:
ROBERTS, M.; BUCHANAN, K.; EVANS, M.; MARIN, R. H.; SATTERLEE D. G.
Revista:
JOURNAL OF EXPERIMENTAL BIOLOGY
Editorial:
The Company of Biologists Limited, Cambridge
Referencias:
Año: 2009 vol. 212 p. 3125 - 3131
ISSN:
0022-0949
Resumen:
The immunocompetence handicap hypothesis (ICHH) suggests that the male sex hormone testosterone has a  ddd dual effect; it controls the development and expression of male sexually selected signals, and it suppresses the immune system. Therefore only high quality males are able to fully express epigamic traits because only they can tolerate the immunosuppressive qualities of testosterone. A modified version of the ICHH suggests that testosterone causes immunosuppression indirectly by increasing the stress hormone corticosterone (CORT).  Lines of Japanese quail (Coturnix japonica) selected for divergent responses in levels of plasma CORT were used to test between these hypotheses. Within each CORT response line (as well as in a control stock) we manipulated levels of testosterone in castrated quail by treatment with zero (sham), low, or high testosterone implants, before testing the birds’ humoral and PHA- induced immune responses, as well as body condition. The PHA- induced response was not significantly affected by CORT selected line, testosterone treatment or their interaction. There was, however, a significant effect of CORT line on humoral immunity such that the control birds exhibited the greatest antibody production, but there was no significant effect of testosterone manipulation on humoral immunity. The males in the sham implant treatment group had significantly greater mass than the males in the high testosterone group, suggesting a negative effect of high testosterone on general body condition. These results are not consistent with the predictions of either of the hypotheses under test and therefore provide no support for either the ICHH or the stress-mediated ICHH.