File Name: stress and immune system .zip
Stress Challenges and Immunity in Space pp Cite as. Research over the past three to four decades has clearly established that psychological stress affects clinically relevant immune system outcomes, including inflammatory processes, wound healing, and responses to infectious agents and other immune challenges e. Individuals vary in their ability to cope with stressful life events, and differences in perceptions of stress, mood e. In this chapter, we provide an overview of key findings linking everyday stressors to immune function and health.
In addition, the complexity of a plausible mechanism through which chronic stress and elevated inflammation might result in serious health consequences including cardiovascular disease, diabetes, and cancer is delineated. The literature provides support for several promising avenues for interventions to prevent stress-induced immune dysregulation. Research examining stressors in everyday life also has strong implications with respect to understanding the effects of more extreme stressors, such as those encountered during space flight, a complex environmental, physiological, and psychological challenge with multiple adverse consequences for human health.
The central nervous system CNS , endocrine system, and immune system are complex systems that interact with each other. Stressful life events and the negative emotions they generate can dysregulate the immune response by disturbing the sensitive interplay among these systems Glaser and Kiecolt-Glaser Psychoneuroimmunology PNI is a field of investigation concerned with the interactions of psychological factors with the neuroendocrine and immune system and consequences for higher brain function and human behavior Dantzer Individual differences exist in the extent to which people mount a physiological stress response.
Individual differences in stress physiology are, among other things, related to the brain, which plays a critical role in appraising stressors, as well as in modulating immune system reactivity to physical and social threats Slavich and Irwin Additionally, certain characteristics of a situation are associated with greater stress responses, including the intensity, severity, controllability, and predictability of the stressor.
Physiological reactivity to stressors are commonly observed even after repeated exposure to the same stressor Dhabhar The autonomic nervous system ANS and the hypothalamic-pituitary-adrenal HPA axis are two major stress-signaling pathways that contribute to immune dysregulation Glaser and Kiecolt-Glaser Experiencing a stressful situation, as perceived by the brain, activates the HPA axis and the sympathetic-adrenal medullary axis SAM , which provokes the release of hormones which modulate immune function including adrenocorticotropic hormone ACTH , cortisol, growth hormone, prolactin, epinephrine, and norepinephrine Glaser and Kiecolt-Glaser see Chap.
Immunity is the natural or acquired resistance of an organism to bacterial or viral invaders, diseases, or infections, while having adequate tolerance to avoid allergy, and autoimmune diseases.
Lymphocytes, including T and B cells are the main type of cells of the immune system. T cells orchestrate the immune response via the production of cytokines and stimulate B cells to produce antibodies and signal killer cells to destroy the antigen-displaying cell Sompayrac Typically, type 1 cytokines favor the development of a strong cellular immune response, whereas type 2 cytokines favor a strong humoral immune response Spellberg and Edwards Jr.
A primary focus of the field of psychoneuroimmunology has been to understanding the link between stress and inflammatory responses. Chronic inflammation secondary to long-term stress has been causally linked with risk for numerous diseases, including infectious illnesses, cardiovascular disease, diabetes, certain cancers, and autoimmune disease, as well as general frailty and mortality Glaser and Kiecolt-Glaser ; Dhabhar ; Padro and Sanders ; Webster Marketon and Glaser One potential explanation for the mechanism linking chronic stress and inflammation in the onset of a wide range of diseases is that prolonged stressors result in glucocorticoid receptor resistance, which, in turn, causes dysregulated HPA axis function and interferes with the appropriate regulation of inflammation Cohen et al.
Animal models have provided compelling evidence that biobehavioral stress mechanisms and their molecular and cellular pathways can cause illness behavior and illness itself. These experimental studies have conclusively demonstrated that exposure to restraint stress triggers exaggerated inflammatory responses Korte et al. These experiments highlight how conditions of chronic inflammation can induce sickness and depressive-like behaviors in response to chronic stress Dantzer et al.
Wound healing is a vitally important process during recovery from either injury or surgery. Converging evidence from observational, experimental, and interventional studies implies that stress and other behavioral factors can impede wound healing processes and compromise immunity via multiple physiological pathways Kiecolt-Glaser et al. Wound healing progresses through several sequential and overlapping phases, including inflammation, proliferation, and regeneration.
Cellular immunity plays an important role in the regulation of wound healing through the production of proinflammatory cytokines and chemokines e. These factors act as chemo-attractants for the migration of phagocytes and other cells to the wound site, starting the proliferative phase which involves the recruitment and replication of cells necessary for tissue regeneration and capillary regrowth Gethin Inflammation is a prerequisite to healing.
Proinflammatory cytokines help to protect against infection and prepare injured tissue for repair by enhancing the recruitment and activation of phagocytes. Unfortunately, stress disrupts the production of proinflammatory cytokines that are essential for wound healing and, when dysregulated, impose a considerable delay in wound repair Gouin and Kiecolt-Glaser The clinical relevance of the relationship between stress and impaired wound healing has been demonstrated in several studies.
A meta-analysis Walburn et al. These results confirm earlier findings by Kiecolt-Glaser et al. Surgical complications e. In an observational study involving patients undergoing coronary artery bypass graft CABG surgery, individuals with more depressive symptoms at discharge had more infections and poorer wound healing over the first six weeks following surgery than individuals who reported less distress Doering et al.
In addition, the pain associated with surgery can itself generate psychological distress, which has been shown to further influence wound healing. A prospective study involving 17 women who underwent elective gastric bypass surgery revealed that greater acute pain immediately after surgery and persistent pain in the four weeks following surgery both were associated with slower healing McGuire et al.
In summary, acute and chronic stressors can negatively impact the wound healing process, by interrupting the inflammatory cascade that is fundamental for wound repair.
Stress can also dysregulate humoral and cellular immune responses to pathogens, increasing risk for infectious illnesses including influenza and the common cold Glaser and Kiecolt-Glaser The association between psychological stress and susceptibility to the common cold has long been recognized; stress suppresses the host resistance to infection and increases rates of infection Cohen et al.
Loneliness is another well-established risk factor for poor physical health. In a study of our own, we were able to demonstrate that loneliness predicts self-reported cold symptoms after a viral challenge, suggesting that cold symptoms are more severe among those who feel lonely LeRoy et al.
Vaccination against influenza virus reduces both risk and severity of infection, thus decreasing risk for hospitalization and death. Vaccine effectiveness is of particular importance among high-risk groups, including pregnant women and older adults.
However, the protective efficacy of antiviral vaccines depends upon their ability to induce both humoral and cell-mediated immune responses Lambert et al. Furthermore, psychological distress and biobehavioral vulnerabilities, which arise from being older or sedentary, have independently been found to alter immune responses to influenza vaccination Segerstrom et al. Interestingly, a 4-week massage intervention in students embarking on academic examinations was associated with reduced distress and enhanced antibody responses after a hepatitis B vaccine Loft et al.
Positive effects of other mind-body therapies, including Tai Chi, Qi Gong, meditation, and Yoga, on the immune system and virus-specific antibody responses to vaccines have also been documented in a meta-analysis of 34 studies Morgan et al. After primary infection, the herpes virus continues to reside in B lymphocytes and white blood cells for the life of the individual. Under normal health conditions, reactivation and replication of the EBV virus is prevented by the cellular immune system, largely orchestrated through specific-memory cytotoxic T cells and natural killer NK ; thus, individuals with herpesvirus infections generally remain asymptomatic Glaser et al.
However, under stressful conditions, suppressive immune activity may be reduced, permitting reactivation of the virus. The relationships between neuroendocrine activity, immune function, and latent HSV type 1 reactivation were initially documented in animal studies.
Among mice infected with HSV type 1, those exposed to a stressor exhibited reactivation of the latent virus, whereas nonstressed mice did not Padgett et al. Today, a body of literature in humans confirms that psychosocial stressors predict reactivation of latent viruses see Chap. For instance, higher self-reported health was associated with lower reactivation of latent herpesviruses and inflammation Murdock et al.
Meanwhile, increased antibody titers against EBV viral capsid antigen VCA have been observed in the context of depression Bennett et al. Together, these human and animal studies show that stress can modulate the steady-state expression of latent herpesviruses, downregulating specific T-cell responses to the virus to an extent that is sufficient to result in viral activation.
Human immunodeficiency virus HIV is similar to herpes viruses, in that the virus remains in a latent state in the body after primary infection. As individuals infected with HIV may have lowered levels of T cells, cells that are important to fight infections, much interest exists in whether chronic stress and depression—that also are known to suppress the human immune system—may affect HIV disease progression. Indeed, there is a substantial body of evidence pointing at a relationship between chronic stress and the rate of HIV disease progression.
Major depression is highly prevalent among HIV-positive patients. Depression is associated with, among other factors, increased inflammatory markers e. These findings are corroborated by a study that investigated norepinephrine, cortisol, depression, hopelessness, coping, and life event stress as predictors of HIV progression in a diverse subject sample every 6 months over a period of 4 years.
The authors found that norepinephrine, depression, hopelessness, and avoidant coping significantly predicted a greater rate of decrease in CD4 and increase in viral load, demonstrating a robust effect of chronic stress on HIV disease progression Ironson et al. In summary, stress can not only increase susceptibility to illness after exposure to infectious agents but also can inhibit antibody and virus-specific T cell responses to vaccines, permit reactivation of latent herpesviruses, and influence the progression of HIV-related disease.
Cardiovascular disease CVD is a major cause of morbidity and mortality. Chronic low-grade inflammation is implicated in the link between stress and CVD via contributions to the early emergence, progression, and thrombotic complications of atherosclerosis Liu et al. IL-6 and CRP, two important biomarkers of inflammation, are thought to be indicative and potentially predictive of atherosclerosis Nadrowski et al. Of clinical importance, the biological effects of stress do not exist in isolation, and are often aggravated by unhealthy behaviors including poor diet, inadequate physical activity, tobacco use, and poor adherence to medication Lagraauw et al.
Epidemiological research over the last half-century has conclusively linked chronic stress and other psychosocial factors to the increased incidence of coronary artery disease von Kanel For instance, individuals exposed to work-related stressors including shiftwork, workplace conflict, and positions typified by high demands combined with low control, exhibit risk for elevations in serum CRP and IL-6 von Kanel et al.
Furthermore, evidence suggests that childhood adversity, particularly severe physical and sexual abuse, confers risk for cardiovascular events, particularly among women Garad et al. These results shed light on potential epigenetic mechanisms that could link childhood adversity to disproportionally elevated risks of inflammatory disease in adulthood. Type-2 diabetes mellitus T2DM is a chronic metabolic disorder that results from defects in insulin secretion and insulin action Hackett and Steptoe Though limited, an emerging body of literature suggests that stress plays a role in the etiology of T2DM, both as a predictor of new-onset T2DM and as a prognostic factor in individuals with existing T2DM Hackett and Steptoe Stress-related biological pathways, including chronic activation of the HPA axis, which can lead to dysregulated cortisol output and neuroendocrine dysfunction, have been conjectured to contribute to the pathogenesis of T2DM Hackett and Steptoe For instance, insulin resistance frequently develops during acute or chronic stress Tsuneki et al.
Moreover, obesity commonly co-occurs in patients with T2DM, and visceral adipose tissue e. Stress exposure during childhood has also been found to constitute a risk factor for obesity and diabetes.
Likewise, a review of literature revealed a significant association between exposure to childhood adversity and an increased risk of T2DM in adulthood Huffhines et al. Of particular note, stress can perinatally impair metabolic health in later life.
However, the mechanisms for this effect are not yet fully understood. One novel potential pathway linking maternal and child weight is the transmission of obesogenic microbes from mother to child Galley et al.
Stress hormones e. Thus, via adrenergic- and glucocorticoid-mediated mechanisms, sympathetic nervous system SNS -activation may alter immune defenses mechanisms and anti-tumor immune capabilities with implications for tumor progression Antoni et al. For instance, exposure to chronic stress Lamkin et al. Correspondingly, increased catecholamine levels have been linked to T lymphocyte apoptosis Radojevic et al.
It has become clear that cancer-related systemic inflammation is associated with poor outcomes, independent of tumor stage Dolan et al. The immune system plays a critical role in the occurrence and progression of immunogenic tumors, including skin cancer Song et al. Furthermore, immunosuppression, such as in solid-organ transplant recipients and patients with human immunodeficiency virus HIV or hematologic malignant neoplasms, has been clearly linked with increased incidence of non-melanoma skin cancer, including BCC, and squamous cell carcinoma Song et al.
Importantly, chronic stress can alter the anti-tumor-specific immune response to immunogenic tumors. Animal models support these findings; mice under restraint stress developed ultraviolet-light Illi et al.
Taken together, these preclinical and clinical studies provide evidence that behavioral stressors can influence the tumor microenvironment. While much initial work focused on direct effects of catecholamines and other stress mediators on cancer progression, subsequent work identified that the tumor microenvironment is a critical regulator of cancer progression and metastasis Landskron et al.
The tumor microenvironment has a pivotal role in regulating tumor cell growth, invasion, and metastasis, specifically through reciprocal cross-talk with infiltrating immune cells lymphocytes, neutrophils, and macrophages , endothelial cells, mesenchymal stromal cells fibroblasts and myofibroblasts , and their secretory products, all of which can modulate gene expression and alter the behavior of tumor cells Mostofa et al.
Acute stress increases resistance to infection. The alteration of this mechanism in chronically stressed people impairs the organism's ability to mount a strong immune response with a resultant increase in morbidity. Protracted stressful conditions decrease NK cytotoxic capacity. There is a substance P, which under stressful circumstances mediates the increase in macrophage cytokine production. Acute stress increases T cell mobilization through a beta2—adrenergically mediated process, which is blunted during chronic stress. Psychological stress impairs the immune system's ability to produce antibodies in response to a vaccine, thereby making the organism more vulnerable to infections. Nowadays it is a proven fact that psychological stress increases the susceptibility to inflammatory disorders, including those of infectious etiology [ 1 , 2 , 3 ].
Not a MyNAP member yet? Register for a free account to start saving and receiving special member only perks. William R. Beisel 1. The interacting responses of the endocrine and immune systems characterize various forms of stress.
One specific focus of this research is to study the effects of stress on the immune systems; after all, if stress affects immunity, that would be one way in which stress.
Stress Challenges and Immunity in Space pp Cite as. Research over the past three to four decades has clearly established that psychological stress affects clinically relevant immune system outcomes, including inflammatory processes, wound healing, and responses to infectious agents and other immune challenges e. Individuals vary in their ability to cope with stressful life events, and differences in perceptions of stress, mood e.
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