Psychological Stress and the Immune System

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:tiphat: to GS for helping gather these studies

Stress and cancer:
The body responds to stress by releasing stress hormones, such as epinephrine (adrenaline) and cortisol (hydrocortisone). Stress hormones increase blood pressure, heart rate, and blood sugar levels. Small amounts of stress are believed to be beneficial, but chronic (persisting or progressing over a long period of time) high levels of stress are thought to be harmful.

More recent research with animal models suggests that the body?s neuroendocrine response (release of hormones into the blood in response to stimulation of the nervous system) can directly alter important processes in cells that help protect against the formation of cancer, such as DNA repair and the regulation of cell growth.

Scientists have suggested that the effects of stress on the immune system may in turn affect the growth of some tumors. However, recent research using animal models indicates that the body?s release of stress hormones can affect cancer cell functions directly.
http://www.cancer.gov/cancertopics/factsheet/Risk/stress

Experimental stress in inflammatory rheumatic diseases: a review of psychophysiological stress responses
Sabine JM de Brouwer,1 Floris W Kraaimaat,1 Fred CGJ Sweep,2 Marjonne CW Creemers,3 Timothy RDJ Radstake,3 Antoinette IM van Laarhoven,1 Piet LCM van Riel,3 and Andrea WM Evers1
In summary, this review shows that there is limited evidence that autonomic and neuroendocrine function is altered after physical or psychological stress in patients with inflammatory rheumatic diseases compared with healthy subjects. In contrast, there is evidence that immune function is altered by stress in a manner specific to different rheumatic diseases, and thus real-life stressors could contribute to the maintenance or exacerbation of rheumatic diseases.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2911873/?tool=pmcentrez

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry
Suzanne C. Segerstrom and Gregory E. Miller
Acute stressors (lasting minutes) were associated with potentially adaptive upregulation of some parameters of natural immunity and downregulation of some functions of specific immunity. Brief naturalistic stressors (such as exams) tended to suppress cellular immunity while preserving humoral immunity. Chronic stressors were associated with suppression of both cellular and humoral measures

In contrast, studies of vulnerable populations such as people with HIV have shown changes in immunity to predict disease progression (Bower et al., 1998).

For example, chronic stressors reliably diminish the immune system?s capacity to produce antibodies following routine influenza vaccinations (see Table 7). Yet as far as we are aware, none of these studies has tracked illness to explore whether stress-related disparities in vaccine response might be sufficient to heighten susceptibility to clinical infection with influenza.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1361287/

Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection and Immunopathology
Firdaus S. Dhabhar
Stress has long been suspected to play a role in the etiology of many diseases, and numerous studies have shown that stress can be immunosuppressive and hence may be detrimental to health. Moreover, glucocorticoid stress hormones are widely regarded as being immunosuppressive, and are used clinically as anti-inflammatory agents.

However, studies have shown that the acute stress response may play a critical adaptive and protective role, with stress hormones and neurotransmitters preparing the immune system for potential challenges (e.g. wounding or infection) that are perceived by the brain (e.g. the detection of predator or attacker).


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2790771/?tool=pmcentrez

The effect of stress on the defense systems
D Dragos and MD Tansescu
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. Acute stress induces a probable sympatho?adrenergically mediated increase in chemotaxis and adhesion molecules expression, thus promoting immune cells migration to sites of infection and/or inflammation, while chronic stress impairs this mechanism. 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.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3019042/?tool=pmcentrez

Modern approaches to understanding stress and disease susceptibility: A review with special emphasis on respiratory disease
Palok Aich, Andrew A Potter, and Philip J Griebel
(Discussion on Stress and disease, Stress and viral infection, Stress and immunity, Mechanism of stress-induced infection susceptibility, etc.)
There are reports which have shown direct connections between stress and immune system function. Similarly, other studies have shown that social stressors could also increase the risk for upper respiratory infection. A viral challenge study provides the strongest evidence for a link between stress and susceptibility to the common cold. Other studies have extended these results by considering a wider range of psychosocial factors.

Human subjects under high stress were shown to be more susceptible to infection with common cold viruses. Furthermore, a diversity of experimental animal models confirmed that laboratory stressors such as forced exercise, avoidance learning, restraint, isolation and cold exposure made animals more susceptible to primary infection with a variety of viruses and bacteria.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840576/?tool=pmcentrez

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Numerous other studies on this subject at PubMed
http://www.ncbi.nlm.nih.gov/pmc/?term=stress+and+the+immune+system

 

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Re: Psychological Stress and the Immune System

Chronic heat stress weakened the innate immunity and increased the virulence of highly pathogenic avian influenza virus H5N1 in mice
Jin Y, Hu Y, Han D, Wang M.
Abstract
Chronic heat stress (CHS) can negatively affect immune response in animals. In this study we assessed the effects of CHS on host innate immunity and avian influenza virus H5N1 infection in mice. Mice were divided into two groups: CHS and thermally neutral (TN). The CHS treatment group exhibited reduced local immunity in the respiratory tract, including the number of pulmonary alveolar macrophages and lesions in the nasal mucosa, trachea, and lungs. Meanwhile, CHS retarded dendritic cells (DCs) maturation and reduced the mRNA levels of IL-6 and IFN-β significantly (P < .05). After the CHS treatment, mice were infected with H5N1 virus. The mortality rate and viral load in the lungs of CHS group were higher than those of TN group. The results suggest that the CHS treatment could suppress local immunity in the respiratory tract and innate host immunity in mice significantly and moderately increased the virulence in H5N1-infected mice.
http://www.ncbi.nlm.nih.gov/pubmed/21687549

Stressor-induced alterations of adaptive immunity to vaccination and viral pathogens
Powell ND, Allen RG, Hufnagle AR, Sheridan JF, Bailey MT.
Abstract
The stress response influences the immune system, and studies in laboratory animals indicate that the response to stress significantly reduces resistance to infectious challenge. Only a few studies, however, have determined the impact of the stress response on human susceptibility to infectious challenge due, in part, to the difficulties of using live, replicating pathogens in human research. As a result, many studies have assessed the immune response to vaccination as a surrogate for the immune response to an infectious challenge. Thus, much is known about how the stress response influences adaptive immunity, and memory responses, to vaccination. These studies have yielded data concerning the interactions of the nervous and immune systems and have provided important information for clinicians administering vaccines to susceptible populations. This review provides a brief overview of the immune response to commonly used vaccines and the impact that stress can have on vaccine-specific immunity.
http://www.ncbi.nlm.nih.gov/pubmed/21094924

Influenza virus-specific immunological memory is enhanced by repeated social defeat.
Mays JW, Bailey MT, Hunzeker JT, Powell ND, Papenfuss T, Karlsson EA, Padgett DA, Sheridan JF.
Abstract
Immunological memory (MEM) development is affected by stress-induced neuroendocrine mediators. Current knowledge about how a behavioral interaction, such as social defeat, alters the development of adaptive immunity, and MEM is incomplete. In this study, the experience of social disruption stress (SDR) prior to a primary influenza viral infection enhanced the frequency and function of the T cell memory pool. Socially stressed mice had a significantly enlarged population of CD8(+) T cells specific for the immunodominant NP366-74 epitope of A/PR/8/34 virus in lung and spleen tissues at 6-12 wk after primary infection (resting memory). Moreover, during resting memory, SDR-MEM mice responded with an enhanced footpad delayed-type hypersensitivity response, and more IFN-gamma-producing CD4(+) T cells were detected after ex vivo stimulation. When mice were rechallenged with A/PR/8/34 virus, SDR-MEM mice terminated viral gene expression significantly earlier than MEM mice and generated a greater D(b)NP(366-74)CD8(+) T cell response in the lung parenchyma and airways. This enhancement was specific to the T cell response. SDR-MEM mice had significantly attenuated anti-influenza IgG titers during resting memory. Similar experiments in which mice were primed with X-31 influenza and challenged with A/PR/8/34 virus elicited similar enhancements in the splenic and lung airway D(b)NP(366-74)CD8(+) T cell populations in SDR-MEM mice. This study demonstrates that the experience of repeated social defeat prior to a primary viral infection significantly enhances virus-specific memory via augmentation of memory T cell populations and suggests that social stressors should be carefully considered in the design and analysis of future studies on antiviral immunity.
http://www.ncbi.nlm.nih.gov/pubmed/20083672

Bereavement and marriage are associated with antibody response to influenza vaccination in the elderly
http://www.ncbi.nlm.nih.gov/pubmed/16198083

Stress-induced modulation of NK activity during influenza viral infection: role of glucocorticoids and opioids.
http://www.ncbi.nlm.nih.gov/pubmed/15664788

Enhancement of antibody responses to influenza vaccination in the elderly following a cognitive-behavioural stress management intervention.
http://www.ncbi.nlm.nih.gov/pubmed/12920328

 

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Re: Psychological Stress and the Immune System

Short natural sleep is associated with higher T cell and lower NK cell activities.
Fondell E, Axelsson J, Franck K, Ploner A, Lekander M, B?lter K, Gaines H.
Abstract
Short sleep duration increases the risk of several diseases, possibly involving compromised immune function. However, most previous studies are based on experimentally induced sleep deprivation, and only a few have studied natural variations in sleep duration. Thus our aim was to study how natural variations in sleep duration affect immune function. In total, 36 healthy men and women, aged 20-54, donated blood; 29 on three consecutive mornings, and seven on one morning. Each morning, participants self-reported sleep duration the night prior to blood draw. General sleep patterns, physical activity and stress were also assessed. A flow-cytometric assay was used to measure natural killer cell activity (NKCA), T cell function (in response to PHA, influenza, and SEA+B), and B cell function (in response to PWM) per volume whole blood. Short sleep duration prior to blood draw (<7 h) was associated with 49% higher PHA-induced T cell function (95% CI 7/109%) and 30% lower NKCA compared with normal prior sleep (7-9 h) (95% CI -46/-8%). In addition, high perceived stress was associated with 39% higher PHA-induced T cell function (95% CI 0/94%). High general physical activity was associated with 47% increased numbers of B cells and 28% increased numbers of T cells, but not with immune function. Our results suggest strong relationships between short sleep duration and T- and NK-cell functions. The stability of the findings as well as the clinical consequences of the link between short sleep and immune function should be explored in future studies.
http://www.ncbi.nlm.nih.gov/pubmed/21496482

Loneliness, social network size, and immune response to influenza vaccination in college freshmen
Pressman SD, Cohen S, Miller GE, Barkin A, Rabin BS, Treanor JJ.
Abstract
Antibody response to the influenza immunization was investigated in 83 1st-semester healthy university freshmen. Elevated levels of loneliness throughout the semester and small social networks were independently associated with poorer antibody response to 1 component of the vaccine. Those with both high levels of loneliness and a small social network had the lowest antibody response. Loneliness was also associated with greater psychological stress and negative affect, less positive affect, poorer sleep efficiency and quality, and elevations in circulating levels of cortisol. However, only the stress data were consistent with mediation of the loneliness-antibody response relation. None of these variables were associated with social network size, and hence none were potential mediators of the relation between network size and immunization response.
http://www.ncbi.nlm.nih.gov/pubmed/15898866

Psychological stress and antibody response to influenza vaccination: when is the critical period for stress, and how does it get inside the body?
Miller GE, Cohen S, Pressman S, Barkin A, Rabin BS, Treanor JJ.
Abstract
OBJECTIVES: This study attempted to determine whether stress of moderate intensity could modulate the antibody response to an influenza vaccination in healthy young adults, identify critical periods during which stress could influence antibody response, and delineate behavioral and biological pathways that might explain relations between stress and antibody.

METHODS: A cohort of 83 healthy young adults underwent 13 days of ambulatory monitoring before, during, and after vaccination. Four times daily, subjects reported the extent to which they felt stressed and overwhelmed and collected a saliva sample that was later used to measure cortisol. A battery of health practices (cigarette smoking, alcohol use, physical activity, sleep hygiene) was assessed daily. Antibody titers to the vaccine components were measured at baseline and at 1-month and 4-month follow-up assessments.

RESULTS AND CONCLUSIONS: To the extent that they reported higher levels of stress across the monitoring period, subjects exhibited poorer antibody responses to the New Caledonia strain of the vaccine. Stress ratings on the 2 days before the vaccine and the day it was given were not associated with antibody response. However, the 10 days afterward appeared to be a window of opportunity during which stress could shape the long-term antibody response to varying degrees. With respect to potential mediating pathways, little evidence emerged in favor of cortisol secretion, alcohol consumption, physical activity, or cigarette smoking. However, analyses were consistent with a pattern in which feelings of stress and loss of sleep become locked into a feed-forward circuit that ultimately diminishes the humoral immune response. These findings may shed light on the mechanisms through which stress increase vulnerability to infectious disease.
http://www.ncbi.nlm.nih.gov/pubmed/15039506