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Stress triggers a coordinated physiological response involving the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis. This dual activation ensures that the body is prepared for both immediate and prolonged stress management. The process begins with the perception of a stressor. This initial phase activates the SNS, leading to the rapid release of adrenaline (epinephrine) from the adrenal glands.
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Related Experiment Video

Updated: Jul 12, 2026

The Trier Social Stress Test Protocol for Inducing Psychological Stress

The Trier Social Stress Test Protocol for Inducing Psychological Stress

Published on: October 19, 2011

Stress system--organization, physiology and immunoregulation.

Ilia J Elenkov¹, George P Chrousos

¹Institute of Neurobiology and Molecular Medicine, Italian National Research Council, Rome, Italy.

Neuroimmunomodulation

|August 22, 2007

Summary

Stress hormones, like glucocorticoids and catecholamines, modulate immune responses. While often seen as immunosuppressive, they can protect against excessive inflammation by shifting immune responses, but may also contribute to chronic inflammatory diseases.

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Last Updated: Jul 12, 2026

The Trier Social Stress Test Protocol for Inducing Psychological Stress

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Published on: October 19, 2011

Restraint to Induce Stress in Mice and Rats

Restraint to Induce Stress in Mice and Rats

Published on: December 6, 2024

Area of Science:

Neuroendocrinology
Immunology
Physiology

Background:

Stress threatens homeostasis, engaging the stress system involving hormones like glucocorticoids and catecholamines.
These stress hormones significantly impact immune functions, including leukocyte activity and cytokine secretion.
The interplay between stress and immunity is complex, influencing T helper cell responses.

Purpose of the Study:

To elucidate the multifaceted effects of stress hormones on the immune system.
To explore the dual role of stress in modulating both systemic and local inflammatory responses.
To investigate the potential contribution of stress system dysregulation to chronic inflammatory diseases.

Main Methods:

Review of existing literature on stress physiology and immunomodulation.
Analysis of the effects of glucocorticoids and catecholamines on immune cell functions.
Examination of the corticotropin-releasing hormone-mast cell-histamine axis in local inflammatory contexts.

Main Results:

Systemically, stress hormones inhibit pro-inflammatory (Th1) responses and promote anti-inflammatory (Th2) shifts.
Locally, stress hormones can enhance pro-inflammatory cytokine production and activate specific immune pathways.
Evidence suggests stress hormones do not uniformly suppress immunity but rather orchestrate complex immune adjustments.

Conclusions:

Stress hormones exhibit a dual effect on immunity, inhibiting systemic inflammation while potentially promoting local inflammation.
Dysregulation of the stress system, involving impaired anti-inflammatory feedback or heightened local responses, may contribute to chronic inflammation and immune disorders.
Understanding this complex relationship is crucial for developing therapeutic strategies for immune-related diseases.