Abstract
Glucocorticoid steroids modulate immunocompetence in complex ways with both immunoenhancing and immunosuppressive effects in vertebrates exposed to different stressors. Such bimodal effects have been associated with variation in duration and intensity of the stress response. Given that natural populations have been exposed to a multitude of stressors, a better understanding of the functional association between duration and intensity of the stress response, the resulting changes in glucocorticoid plasma levels and their impact on different aspects of immunocompetence emerges as a cornerstone for vertebrate conservation strategies. We investigated the effects of a restraint challenge (with and without movement restriction), long-term captivity, and transdermal corticosterone application on plasma levels of corticosterone (hereinafter referred to as CORT) and different parameters of innate immunocompetence in the male cururu toads (Rhinella icterica). We show that for R. icterica restraint for 24h proved to be a stressful condition, increasing CORT by 3-fold without consistent immunological changes. However, the application of a more intense stressor (restraint with movement restriction), for the same period, potentiated this response resulting in a 9-fold increase in CORT, associated with increase Neutrophil/Lymphocyte ratio (N:L) and a lower bacterial killing ability (BKA). Transdermal application of corticosterone efficiently mimics repeated acute stress response events, without changing the immune parameters even after 13 days of treatment. Interestingly, long-term captivity did not mitigate the stress response, since the toads maintained 3-fold increased CORT even after 3 months under these conditions. Moreover, long-term captivity in the same condition increased total leukocyte count (TLC) and generated an even greater decrease in BKA, suggesting that consequences of the stress response can be aggravated by time in captivity.
Highlights
Glucocorticoid hormones are produced by adrenal or interrenal glands, and their release is modulated by several stressors through the activation of the hypothalamic pituitary-interrenal axis (HPI) inectotherms vertebrates [1]
The immunosuppressive effects of glucocorticoids have been more commonly observed in contexts of intense and chronic activation of the HPI axis
Immune-enhancing effects have been very commonly observed in the context of low-intensity and short-term activation of the HPI axis, include an increased expression of receptors for different cytokines [6], and redistribution of immune cells within the body, with corresponding increased traffic of leukocytes and enhanced immune function in organs such as the skin [7,8]
Summary
Glucocorticoid hormones are produced by adrenal or interrenal glands, and their release is modulated by several stressors through the activation of the hypothalamic pituitary-interrenal axis (HPI) inectotherms vertebrates [1]. The immunosuppressive effects of glucocorticoids have been more commonly observed in contexts of intense and chronic activation of the HPI axis These immunosuppressive effects include inhibition of the synthesis, release and efficiency of several cytokines and other mediators that promote the immune response and inflammatory reactions, and atrophy of lymphoid tissues, the thymus [1,6]. Studies have identified mechanisms involving dendritic cell, neutrophil, macrophage, and lymphocyte trafficking, maturation, and function through which acute stressors may enhance innate as well as adaptive immunity [7,8] This bimodal effect of glucocorticoids on the immune response can be mediated by different concentrations of these hormones and possibly different receptors [6,9,10,11]. These hormones decrease the T-cell response at high concentration, an effect possibly mediated through glucocorticoid receptors [9,10,11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
