Impact of Human Stress Response on Immune System



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Impact of Human Stress Response on Immune System


Stress puts a strain on the adaptive ability of an organism to deal with the environment, leading to biological changes and psychological demands that might increase the risk of the organism becoming ill (Goliszek 2014). Our reaction to stress influences the ability to avoid diseases and illnesses induced by it. This is an indication that we have the potential to influence how we react to stressful life situations and with it, the overall general wellbeing of our immune system. While there are various forms of stress in life, the three key perspectives or theories of stress are psychological stress, environmental stress and biological stress.  The psychological stress perspective is concerned with people's subjective assessments of their capability to deal with demands that they encounter under certain experiences and situations. The environmental stress context entails an evaluation of environmental experiences or situations that are objectively linked to significant adaptive demands. On the other hand, biological stress context stress on the role of various psychological systems in the human body that are under the regulation of physical and physiological demanding situations (Priyadarshini & Aich 2012). Stress and illnesses share a complex relationship. The level of susceptibility to stress differs from one individual to another. For example, a stressful event might cause an illness to one person but not to another. This is due to an interaction between stressful events and such background factors as coping style, social support, and personality type. In line with these observations, the aim of this essay is to examine the impact of human stress response on the immune system and in particular, how acute and chronic stress affects the immune system, thereby escalating human susceptibility to illnesses.


Interactions between stress and immune system

The complex interactions between an organism's immune system and the CNS (central nervous system is well established (Faith et al., 2006), and the endocrine system is thought to mediate this complex bi-directional interactions. The two vital elements of such interactions include the production of stress hormones courtesy of the HPA (hypothalamic-pituitary-adrenal) axis and the SAM (sympathetic-adrenal-medullary) axis (Hussain, 2010). Cytokines production also triggers the interactions between immune cells. Hormones bind to their receptors and in this way, help to modulate the immune factors. For example, cytokines modulation aids in the feedback to the brain, resulting in HPA axis changes, in addition to inducing such sickness behaviur as loss of appetite, fever, depression, as well as changes in sleep patterns (Goliszek, 2014).  A good example of such feedback loop is via the effect of interleukin-1 (IL-1) on the hypothalamus, thereby inducing the production of CRH (corticotrophin releasing hormone). In this case, the CRH could act on the HPA axis by inducing a rise on levels of stress hormone. While such interactions tend to be very complex, ongoing research work in psychoneuroimmunology is helping to enhance our understanding of the complexities that characterise body/mind interactions (Faith et al., 2006).

Effect of stress on the immune system

Since the immune system is actively involved in defending the body of an organism against other different kinds of organism (Talbott, & Kreamer, 2007), it follows therefore that any changes or abnormalities in the ability of the body's immune system to undertake its normal functions will result in such severe implications as an enhanced risk of mortality or severe illness (Glaser, R & Kiecolt-glaser, 2009), as a result of an infection. Research findings from diverse literature on human subjects and animal models have examined how infectious diseases are related to stress-induced immune dysregulation, and more so with virus infections. The use of mouse models by a number of laboratories has provided important information in exploring these interactions.  A common stressor that researcher conducting stress studies involving mice have come to rely on is restrain stress. In this study, the researchers place the mice under study in plastic tubes to enable backward and forward movement (Jeong, Lee & Kang, 2013). However, the mice cannot turn around. The researchers also make sure that they have drilled holes on the sides of the plastic tubes. This is for purposes of avoiding overheating of the mice, and also to permit air entry. In a succession of studies involving the influenza virus, the research findings indicated that restraint stress changed the adaptive and innate immune responses to the virus. The observed changes in the experiments are such as suppression of anti-inflammatory and proinflammatory cytokines, as well as levels of antibody that the virus produced over a determined period of time. A very interesting observation that the researchers made in these studies is that when they used the RU486 drug that hindered the glucocorticoid receptor from attaching on the lymphocytes, this effectively blocked the effect of stress (O’Mahony et al., 2010). Consequently, the animals resembled their unstressed controls. What such studies seem to indicate is that stress hormones play a key role in regulating general immune response, and modulating response to such infectious pathogens as the influenza virus. 

Theoretical models of stress and immunity-related

Different models have thus far been proposed in an attempt to shed more light on the link between the immune system and stress. Hans Selye is among the first proponents to suggest the three phases of adaptation to stress. The three phases are: alarm, resistance, and exhaustion (Szabo,  Tache & Somogyi, 2012). During the alarm stage, the body is in what is known as a “fight-or-flight” mode in readiness for an impending threat. Should the stressful situation endure, this triggers the resistance stage. During this phase, the body secretes additional blood sugar and hormones as a means of generating enough energy to fight. Should the stressor prolong for a long time, this is likely to trigger the exhaustion phase (Hussain 2010). During this stage, the body is depleted of its reserve immunity and energy. This could cause either an illness or even death. This model has found ideal application in many studies that have also reported a link between chronic stress and the suppression of the lymphocyte responses, and a reduction in natural killer cell. While this immunosuppressant model is still influential globally, newer models have since been developed, such as the biphasic model which considers the kind of stress (chronic or acute) and its impact on the immune response. According to this model, chronic stress has a suppression effect on the immune response, even as chronic stress enhances it. This is because chronic stress both weakens and depletes the resources of the immune response, while acute stress aids in immune cells redistribution in the body, thereby enhancing the efficiency of an organism to fend off potential invaders.

Empirical Evidence on Stress and Immunity

Various studies have reported on the link between immune functions and stress. For example, healthy individuals are reported to experience such immune system impairments as enhanced susceptibility to common colds and fewer immune cells when under stress (Kahan et al. 2009). Decreased functionality and numbers of NK (natural killer) cells have also been reported among students experiencing stress while undertaking their examinations. In the same way, separated or divorced women and men present with poorer immune functions in comparison with their married counterparts. In the same way, persons suffering from PTSD (post-traumatic stress disorder) have been reported to have fewer B-cells, T-cells, and NK cells in comparison with unaffected individual (Glaser, R & Kiecolt-glaser 2009).  There is also evidence in existing literature on stress and immunity of the link between immune functions and perceived stress (Ader 2011). For example, anxiety and psychological distress has been reported to share an inverse correlation with the natural killer cell activity. In the same way, poor response to vaccines has been linked to elevated perception of stress. In addition, women undergoing surgery who experienced high anxiety and depression symptoms were also found to have lower numbers of B cells, T Helper cells, and lymphocytes (Baum, Revenson & Singer, 2012).

Evidence of interaction between the immune and endocrine systems and the CNS stem from observations made by researchers that such neurotransmitters as serotonin, norepinephrine, acetylcholine, and dopamine; neuropeptides like substance P, corticotrophin-releasing factor; neorohormones like adrenocorticotrophin hormone, growth hormone, and prolactin (Brannon, Feist, & Updegraff, 2013); as well as adrenal hormones like epinephrine and corticosteroids affect immune function in vitro and in vivo, and that the receptors for such molecules are to be found on macrophages and lymphocytes (Hussain 2010).  It is also important to note that the immune and neuroendocrine systems share common receptors and mediators, and this is indicative of the immunoregulatory role of the brain. Many studies indicate that the high concentrations of corticosteriods during stress have vital immunosuppressive role on how the macrophages and lymphocytes function and could in fact influence their circulation patterns (Brannon et al., 2013).  Corticosteriods have also been shown to inhibit the production of many mediators and cytokines of inflammation, in addition to reducing the effect of certain inflammatory molecules on specific targeted tissues. Even as acute stress at times enhances the secretion of prolactin and growth hormone, on the other hand, chronic stress is linked to the suppression of the secretion of growth hormone, as well as the suppression of the expression of prolactin mRNA.


Stress has far-reaching detrimental effects on the immune function. While stress is connected to illness, the relationship is quite complex. Owing to the strong inter-relation between immune and endocrine systems, disruption to one owing to emotional or physical stress ends up causing damage to the other. Ongoing stress enhances our susceptibility to diseases and illnesses since the brain signals the endocrine system to release various hormones as a defensive mechanism to the impending threat. While this is desirable in case of a fight-or-flight mode, prolonged stress severely depresses the immune system, thereby triggering the development of various illnesses such as heart disease and cancer. This happens after the defense mechanism triggers the release of chemical reactions that leads to overproduction of the hormone cortisol and other hormones. It also reduces levels of NK cells, and white blood cells, enhance tumor growth and development, in addition to enhancing the rate of tissue damage and infection.













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