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Impacts of Stress: How stress negatively Affects the Immune System

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In the early 19th century, the French physiologist Claude Bernard introduced a theory

suggesting that, as organisms become more independent of their surroundings, they develop

more complex ways of stabilizing their internal environments to counter the changes in their

external environment. Exposure to hostile conditions (usually referred to as stressors) results in a

series of coordinated responses organized to enhance the probability of survival. These collective

responses often referred to as “stress responses,” are composed of alterations in behavior,

autonomic function, and the secretion of multiple hormones, including adrenocorticotropin

hormone (ACTH), and cortisol/corticosterone, adrenal catecholamines, oxytocin, prolactin, and

renin. Stressful experiences can precipitate depression and anxiety, and stress-induced changes in

physiology include an immune component. Individuals vary in their ability to cope with stressful

life events, and differences in perceptions of stress, mood (e.g., depressive symptoms), and

adverse life events can modify the magnitude to which stressors exnegatively influence immune

function.

Throughout the evolution of mammalian physiology, stress-inducing situations reliably

required activation of the immune system and vice versa. As such, the endocrine and the immune

system have become intricately co-regulated, generating a physiological concordance that

subserves vital functions such as regulation of energy allocation, reproduction, learning, mood,

and behavior. Preventing and managing long-term stress can lower your risk for other conditions

like heart disease, obesity, high blood pressure, and depression. This paper aims to demonstrate

that stress negatively affects the immune system. Research over the past three to four decades

has established that psychological stress affects clinically relevant immune system outcomes,

including inflammatory processes, wound healing, and responses to infectious agents and other

immune challenges.
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Although the concept of stress has earned a bad reputation, it is important to recognize

that the adaptive purpose of a physiological stress response is to promote survival during a fight

or flight. While long-term stress is generally harmful, short-term stress can be protective as it

prepares the organism to deal with challenges. Stress responses help your body adjust to new

situations. Stress can be positive, keeping us alert, motivated, and ready to avoid danger. Stress

does not always affect memory. Sometimes, under special conditions, stress can improve

memory. These conditions include non-familiarity, non-predictability, and life-threatening

aspects of imposed stimulation. Under these specific conditions, stress can temporarily improve

the function of the brain and, therefore, memory. In fact, it has been suggested that stress can

sharpen memory in some situations. The process of strengthening memory is usually reinforced

after stress.

Various studies on animal and human models have shown that administration of either

glucocorticosteroids or stress shortly after learning has occurred facilitates memory. Thus, short-

term stress can enhance the acquisition and/or expression of immunoprotective (wound healing,

vaccination, anti-infectious agent, anti-tumor) or immuno-pathological (pro-inflammatory,

autoimmune) responses. short-term stress is one of nature's fundamental but under-appreciated

survival mechanisms that could be clinically harnessed to enhance immunoprotection. Short-

term (i.e., lasting for minutes to hours) stress experienced during immune activation enhances

innate/primary and adaptive/secondary immune responses. Mechanisms of immuno-

enhancement include changes in the dendritic cell, neutrophil, macrophage, and lymphocyte

trafficking, maturation, and function as well as local and systemic production of cytokines. 
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The central nervous system (CNS), endocrine system, and immune system are complex

systems that interact with each other. Stressful life events and their negative emotions can

dysregulate the immune response by disturbing the sensitive interplay among these systems. The

autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal (HPA) axis are two

major stress-signaling pathways contributing to immune dysregulation. Given the well-known

and marked influence of psychological stress on immunity and infection resistance, and the

likely shared mechanisms by which psychological stress and exercise stress alter immunity; i.e.

principally through activation of the hypothalamic-pituitary-adrenal (HPA) axis and

sympathetic-adrenal-medullary (SAM) axis and subsequent immunomodulatory hormones, it has

been hypothesized that psychological stress can play a role in the decrease in immunity with

prolonged heavy exercise and heavy training. Unfortunately, exercise immunologists rarely

report measures of psychological stress in their studies and so there is little by way of empirical

evidence to support this hypothesis

A primary focus of the field of psychoneuroimmunology has been to understand the link

between stress and inflammatory responses. Although acute inflammation is an adaptive

response to physical injury or infection, exaggerated and/or prolonged inflammatory responses

are detrimental to health. Chronic inflammation secondary to long-term stress has been causally

linked with risk for numerous diseases, including infectious illnesses, cardiovascular disease,

diabetes, certain cancers, autoimmune disease, and general frailty and mortality. Animal models

have provided compelling evidence that biobehavioral stress mechanisms and their molecular

and cellular pathways can cause illness behavior and the illness itself. These experimental studies

have conclusively demonstrated that exposure to restraint stress triggers exaggerated

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inflammatory responses. These experiments highlight how conditions of chronic inflammation

can induce sickness and depressive-like behaviors in response to chronic stress.

 The brain is the site at which the effects of stressors are sensed and appropriately coordinated

behavioral and neuroendocrine responses are initiated. Adaptations involving allostasis to cope

with real, simulated, or imagined challenges are determined by genetic, developmental, and

previous experimental factors. While they may be effective for a short interval, the alterations

may have cumulative adverse effects over time. For instance, chronic elevation of blood pressure

ensures adequate blood flow to the brain eventually leading to atherosclerosis and stroke or

coronary occlusion.
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References

Bekhbat, M., & Neigh, G. N. (2018). Sex differences in the neuro-immune consequences of stress:

Focus on depression and anxiety. Brain, behavior, and immunity, 67, 1-12.

https://doi.org/10.1016/j.bbi.2017.02.006 

Bottaccioli, A. G., Bottaccioli, F., & Minelli, A. (2019). Stress and the psyche–brain–immune network

in psychiatric diseases based on psychoneuroendocrineimmunology: a concise review. Annals of

the New York academy of sciences, 1437(1), 31-42. https://doi.org/10.1111/nyas.13728 

Edwards, J., Walsh, N., Diment, B., & Roberts, R. (2018). Anxiety and perceived psychological stress

play an important role in the immune response after exercise. Exercise immunology review, 24. 

http://hdl.handle.net/10316.2/44138

Ray, A., Gulati, K., & Rai, N. (2017). Stress, anxiety, and immunomodulation: a pharmacological

analysis. Vitamins and hormones, 103, 1-25. https://doi.org/10.1016/bs.vh.2016.09.007

Seiler, A., Fagundes, C. P., & Christian, L. M. (2020). The impact of everyday stressors on the immune

system and health. In Stress challenges and immunity in space (pp. 71-92). Springer, Cham.

https://doi.org/10.1007/978-3-030-16996-1_6
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