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1 March 2017 Research Article: The effects of psychological and physical stressors on the secretion of immunoglobulin A in humans and mice
Katey Kohanski, Sarah Beth Redmond
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Abstract

Stress generates multiple physiological effects through activation of neuroendocrine signaling. An increase in the hormone cortisol (or the analog corticosterone in some species), causes a significant decrease in circulating B-lymphocytes (the immune cells that produce antibodies), making the antibody immunoglobulin A (IgA) a good stress marker. The objective of these experiments was to examine IgA secretion after psychological and physical stressor treatments were applied. IgA was extracted from the salivary samples of college students who did or did not have a scheduled exam to test impacts of purely psychological stress, and from fecal samples of mice treated with human handling (psychological stress), forced exercise (physical stress), or a combination of the two. An enzyme-linked immunosorbent assay was used to measure IgA level in each sample. In humans, exam-taking was significantly associated with low salivary IgA levels (p < 0.05), suggesting that the psychological stressor negatively impacted the immune response. In mice, the handling group did not exhibit any significant change in fecal IgA level (p > 0.05), which may or may not have been a result of habituation to handling. However, both the physical stress group and combined physical and psychological stress group exhibited significantly reduced fecal IgA levels (p < 0.05) in comparison to the control. This study supports other findings that different stressors have different effects on physiological markers of stress, such as IgA level, and demonstrates those differences in humans and a controlled model of psychological and physical stressors in mice.

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Katey Kohanski and Sarah Beth Redmond "Research Article: The effects of psychological and physical stressors on the secretion of immunoglobulin A in humans and mice," BIOS 88(1), 1-8, (1 March 2017). https://doi.org/10.1893/BIOS-D-14-00035.1
Received: 4 August 2014; Accepted: 1 December 2015; Published: 1 March 2017
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