Psychological stress and susceptibility to upper respiratory infections (original) (raw)
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Stress, immune reactivity and susceptibility to infectious disease
2002
Psychological stress is known to affect immune function and to predict infectious disease susceptibility. However, not all individuals who are stressed develop disease. In the present article, we report on a series of studies from our laboratory describing interindividual variability of immune responses to psychological stress. In our initial series of experimental investigations, we demonstrated that acute laboratory stress alters both quantitative and functional components of cellular immunity.
Psychological Stress, Cytokine Production, and Severity of Upper Respiratory Illness
Psychosomatic Medicine, 1999
Objective: The purpose of this study is to assess the role of psychological stress in the expression of illness among infected subjects and to test the plausibility of local proinflammatory cytokine production as a pathway linking stress to illness. Methods: After completing a measure of psychological stress, 55 subjects were experimentally infected with an influenza A virus. Subjects were monitored in quarantine daily for upper respiratory symptoms, mucus production, and nasal lavage levels of interleukin (IL)-6. Results: Higher psychological stress assessed before the viral challenge was associated with greater symptom scores, greater mucus weights, and higher IL-6 lavage concentrations in response to infection. The IL-6 response was temporally related to the two markers of illness severity, and mediation analyses indicated that these data were consistent with IL-6 acting as a major pathway through which stress was associated with increased symptoms of illness. However, this pattern of data is also consistent with increases in IL-6 occurring in response to tissue damage associated with illness symptoms. Conclusions: Psychological stress predicts a greater expression of illness and an increased production of IL-6 in response to an upper respiratory infection.
Journal of Psychosomatic Research, 2001
To investigate the efficacy of a stress management programme on symptoms of colds and influenza in 27 university students before and after the examination period. The incidence of symptoms, levels of negative affect, and secretion rate of secretory immunoglobulin A (sIgA) were recorded for 5 weeks before treatment, for the 4 weeks of treatment, and for 8 weeks after treatment in treated subjects and in 25 others who did not participate in stress management. Symptoms decreased in treated subjects but not in controls during and after the examination period. Although sIgA secretion rate increased significantly after individual sessions of relaxation, resting secretion rate of sIgA did not increase over the course of the study. Negative affect decreased after examinations in both groups, but was not affected by treatment. Stress management reduced days of illness independently of negative affect and sIgA secretion rate. Although the component of treatment responsible for this effect has yet to be identified, psychological interventions may have a role in reducing symptoms of upper respiratory tract infection.
Reactivity and Vulnerability to Stress-Associated Risk for Upper Respiratory Illness
2002
We tested the hypothesis that the greater a person's laboratory stress-elicited elevation in cortisol, the greater the life stress-related risk for upper respiratory infection (URI). We also tested the prediction that the greater the laboratory stress-elicited rise in natural killer cell (NK) cytotoxicity, the smaller the life stress-related URI risk. Finally, we explored whether sympathetic nervous system (SNS) and enumerative immune reactivities to laboratory stress moderate the relation between life stress and URI. Methods: At baseline, 115 healthy subjects were administered a negative stressful life events checklist and were tested to assess their SNS (blood pressure, heart rate, and catecholamines), HPA (cortisol), and immune (NK cell cytotoxicity and lymphocyte subsets) reactivities to laboratory speech tasks administered 2 weeks apart. Responses were averaged across the two laboratory assessments to create reactivity scores. After these assessments were completed, participants were followed weekly for 12 consecutive weeks. At each follow-up they completed a measure of perceived stress experienced over the last week. They were also instructed to contact the study coordinator if they had a cold or flu at any time during follow-up. A health care worker verified reported illnesses. Results: In a traditional prospective analysis, high cortisol reactors with high levels of life events had a greater incidence of verified URI than did high reactors with low levels of life events and low reactors irrespective of their life event scores. Using hierarchical linear modeling, CD8 ϩ number, Natural Killer (NK) cell number, and NK cell cytotoxicity, each interacted with weekly perceived stress levels in predicting concurrent occurrences of self-reported URIs. For these outcomes, low immune reactors were more likely to experience an URI during high stress than low stress weeks. High immune reactors did not exhibit differences in weekly URIs as a function of weekly stress level. The SNS reactivity markers did not moderate the association of stress and URI incidence in either analysis. Conclusions: Acute HPA and immune responses to laboratory stressors are markers of how vulnerable people are to the increased risk for URI associated with stressors in the natural environment. Key words: reactivity, cardiovascular, immune, cortisol, upper respiratory illness, common cold.
Psychobiologic Reactivity to Stress and Childhood Respiratory Illnesses
Psychosomatic Medicine, 1995
Psychological stress is thought to undermine host resistance to infection through neuroendocrine-mediated changes in immune competence. Associations between stress and infection have been modest in magnitude, however, suggesting individual variability in stress response. We therefore studied environmental stressors, psychobiologic reactivity to stress, and respiratory illness incidence in two studies of 236 preschool children. In Study 1,137 3-to 5-year-old children from four childcare centers underwent a laboratory-based assessment of cardiovascular reactivity (changes in heart rate and mean arterial pressure) during a series of developmentally challenging tasks. Environmental stress was evaluated with two measures of stressors in the childcare setting. The incidence of respiratory illnesses was ascertained over 6 months using weekly respiratory tract examinations by a nurse. In Study 2, 99 5-year-old children were assessed for immune reactivity (changes in CD4+, CD8 + , and CD19+ cell numbers, lymphocyte mitogenesis, and antibody response to pneumococcal vaccine) during the normative stressor of entering school. Blood for immune measures was sampled 1 week before and after kindergarten entry. Environmental stress was indexed with parent reports of family stressors, and a 12-week respiratory illness incidence was measured with biweekly, parent-completed symptom checklists. The two studies produced remarkably similar findings. Although environmental stress was not independently associated with respiratory illnesses in either study, the incidence of illness was related to an interaction between childcare stress and mean arterial pressure reactivity (/3 = .35, p < .05) in Study 1 and to an interaction between stressful life events and CD19+ reactivity (/3 = .51, p < .05) in Study 2. In both studies, reactive children sustained higher illness rates under high-stress conditions, but lower rates in low-stress conditions, compared with less reactive peers. Stress was associated with increased rates of illnesses, but only among psychobiologically reactive children. Less reactive children experienced no escalation in illness incidence under stressful conditions, suggesting that only a subset of individuals may be susceptible to the health-altering effects of stressors and adversity.
Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry
Psychological Bulletin, 2004
The present report meta-analyzes more than 300 empirical articles describing a relationship between psychological stress and parameters of the immune system in human participants. 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. Effects of event sequences varied according to the kind of event (trauma vs. loss). Subjective reports of stress generally did not associate with immune change. In some cases, physical vulnerability as a function of age or disease also increased vulnerability to immune change during stressors.
Brain, Behavior, and Immunity, 2009
Activation of the innate immune system is commonly accompanied by a set of behavioural, psychological and physiological changes known as 'sickness behaviour'. In animals, infection-related sickness symptoms are significantly increased by exposure to psychosocial stress, suggesting that psychological and immune stressors may operate through similar pathways to induce sickness. We used a double-blind, randomised, placebo-controlled design to examine the effect of acute psychological stress on immune and subjective mood responses to typhoid vaccination in 59 men. Volunteers were assigned to one of four experimental conditions in which they were either injected with typhoid vaccine or saline placebo, and then either rested or completed two challenging behavioural tasks. Typhoid vaccine induced a significant rise in participants' serum levels of interleukin-6 (IL-6) and this response was significantly larger in the stress versus rest conditions. Negative mood increased immediately post-tasks, an effect also more pronounced in the vaccine/stress condition. In the vaccine/stress group, participants with larger IL-6 responses had heightened systolic blood pressure responses to tasks and elevated post-stress salivary levels of the noradrenaline metabolite 3-methoxy-phenyl glycol (MHPG) and cortisol. Our findings suggest that, as seen in animals, psychological and immune stressors may act synergistically to promote inflammation and sickness behaviour in humans.
Stress and Pathogenesis of Infectious Disease
Clinical Infectious Diseases, 1991
Despite inherent difficulties in defining and measuring stress, a scientific framework has been provided in recent years for understanding how disruptive life experiences might be translated into altered susceptibility to infectious diseases. Studies of the effects of stress on pathogenesis of infectious disease are highly relevant to assessment of the biological importance of the immune impairments that have been associated with stress. With a few notable exceptions, investigations of viral infections in humans and in animal models support the hypothesis that stress promotes the pathogenesis of such infections. Similar conclusions can be drawn from studies of bacterial infections in humans and animals and from a small number of studies of parasitic infections in rodent models. While many of these studies have substantial limitations, the data nonetheless suggest that stress is a potential cofactor in the pathogenesis of infectious disease. Given recent unprecedented advances in the neurosciences, in immunology, and in the field of microbial pathogenesis, the relationship between stress and infection should be a fruitful topic for interdisciplinary research.
IMMUNE DYSREGULATION IN HEALTHY MEDICAL STUDENTS DURING EXPOSURE TO ACUTE AND CHRONIC STRESSORS
Psychosomatic Medicine
The mechanisms of stress-related immune alterations have not been fully elucidated. Cell-mediated immune responses as well as antibody and certain cytokines are reported as being suppressed during times of high stress. However, the role of suppression vs dysregulation has not been established in human stress models. The effect of exam stress on regulatory cytokines in 16 healthy medical students was assessed by measuring type-1 (IFN-γ) and type-2 (IL-10) cytokines from 72-h PHA/PMA-stimulated PBMC 4 weeks before and 48 h after exams. Results demonstrated decreased IFN-γ accompanied by increased IL-10 during exam stress that resulted in a decreased IFN-γ : IL-10 ratio. There was a significant correlation between the cytokine response to PHA/PMA and number and subjective adjustment to daily hassles. Additionally, students who reported greater levels of loneliness also reported greater numbers of and poorer subjective adjustment to hassles. The differences were consistent in both males and females but did not correlate with AM cortisol levels. Additionally, when individuals were grouped into high vs low preexam hassle levels, the type-1/type-2 shift in the IFN-γ : IL-10 ratio occurred in the low hassles group only. These data suggest that psychologically stressful situations shift type-1/type-2 cytokine balance toward type-2 and result in an immune dysregulation rather than overall immunosuppression. This may partially explain the increased incidence of type-2-mediated conditions such as increased viral infections, latent viral expression, allergic/asthmatic reactions, and autoimmunity reported during periods of high stress.