Chronic stress increases adaptive immune response over six weeks in the house sparrow, Passer domesticus

• Published in: General and comparative endocrinology 2024-11, Vol.358, p.114612, Article 114612
• Main Authors: Martinez, Viridiana, Duran, Elena M.I., Kimmitt, Abigail A., Russell, Karen E., Jill Heatley, J., Grace, Jacquelyn K.
• Format: Article
• Language: English
• Subjects: Acute stress; Chronic stress; Corticosterone; Heterophil/lymphocyte ratio; House sparrow; Wound healing
• ISSN: 0016-6480; 1095-6840; 1095-6840
• DOI: 10.1016/j.ygcen.2024.114612

•Chronic stressor exposure is associated with stronger adaptive immune responses.•Acute stress is associated with no changes to immune responses.•Within-trait correlations increase with chronic stressor exposure.•Effects of chronic stressor exposure strengthen over time.•Effects of chronic stressor exposure are not apparent until after 20 days. The vertebrate stress response enables an organism to shift energy towards activities that promote immediate survival when facing a threat to homeostasis, but it can also have detrimental effects on organismal health. Acute and chronic stressors generally have contrasting effects on immune responses, but the timeline of this transition between acute and chronic stressors and their effects on immune responses remains unclear. In this study, we investigate changes in immune markers in captive house sparrows (Passer domesticus) after exposure to normal laboratory conditions, an acute stressor, and chronic stressors for 42 days. Specifically, we examined changes in baseline and stress-induced corticosterone concentrations, body condition, heterophil/lymphocyte (H:L) ratio, hemolysis-hemagglutination, and wound healing. We found that individuals exposed to a single acute stressor had significantly higher stress-induced corticosterone concentrations 24 h after stressor exposure, however this effect was reversed after 48 h. Chronic stressor exposure resulted in generally stronger adaptive immune responses, demonstrated by higher baseline and stress-induced lysis, higher baseline hemagglutination, and slower wound healing. Within-trait correlations also increased with chronic stressor exposure, suggesting limitations on phenotypic plasticity. Most of the effects of chronic stressor exposure on immune markers strengthened over the 42 days of the experiment and differences between captivity-only and treatment groups were not apparent until approximately 20 days of chronic stressor exposure. These results highlight the importance of stressor duration in understanding the effects of chronic stressor exposure on immune responses.