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Stress in paradise: effects of elevated corticosterone on immunity and avian malaria resilience in a Hawaiian passerine
Author(s) -
Gabrielle Names,
Elizabeth M. Schultz,
Jesse S. Krause,
Thomas P. Hahn,
John C. Wingfield,
Molly Heal,
Jamie M. Cornelius,
Kirk C. Klasing,
Kathleen E. Hunt
Publication year - 2021
Publication title -
journal of experimental biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.367
H-Index - 185
eISSN - 1477-9145
pISSN - 0022-0949
DOI - 10.1242/jeb.242951
Subject(s) - passerine , malaria , resilience (materials science) , corticosterone , paradise , biology , immunity , zoology , ecology , immunology , immune system , endocrinology , history , hormone , physics , art history , thermodynamics
Vertebrates confronted with challenging environments often experience an increase in circulating glucocorticoids, which result in morphological, physiological and behavioral changes that promote survival. However, chronically elevated glucocorticoids can suppress immunity, which may increase susceptibility to disease. Since the introduction of avian malaria to Hawaii a century ago, low-elevation populations of Hawaii Amakihi (Chlorodrepanis virens) have undergone strong selection by avian malaria and evolved increased resilience (the ability to recover from infection), while populations at high elevation with few vectors have not undergone selection and remain susceptible. We investigated how experimentally elevated corticosterone affects the ability of high- and low-elevation male Amakihi to cope with avian malaria by measuring innate immunity, hematocrit and malaria parasitemia. Corticosterone implants resulted in a decrease in hematocrit in high- and low-elevation birds but no changes to circulating natural antibodies or leukocytes. Overall, leukocyte count was higher in low- than in high-elevation birds. Malaria infections were detected in a subset of low-elevation birds. Infected individuals with corticosterone implants experienced a significant increase in circulating malaria parasites while untreated infected birds did not. Our results suggest that Amakihi innate immunity measured by natural antibodies and leukocytes is not sensitive to changes in corticosterone, and that high circulating corticosterone may reduce the ability of Amakihi to cope with infection via its effects on hematocrit and malaria parasite load. Understanding how glucocorticoids influence a host's ability to cope with introduced diseases provides new insight into the conservation of animals threatened by novel pathogens.

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