Lipid reactivity to stress: I. Comparison of chronic and acute stress responses in middle-aged airline pilots.

Lipids increase during psychological stress, but no studies have compared the effects of acute and chronic stressors on lipid responsivity in the same individuals. One hundred middle-aged men (n?=?92) and women (n?=?8) were examined during high chronic occupational stress, low chronic stress, and acute laboratory stressors. In addition to measures of perceived stress and affect, an extensive battery of lipid and lipoprotein measures was undertaken at each time point. Most lipid parameters were significantly increased during the chronic and acute stressors, although the responses to the different stressors were not consistently associated. For example, significant correlations among the chronic and acute stress responses were apparent for the apoproteins, but not for total, low density lipoprotein, or high density lipoprotein cholesterol. The factors and processes regulating these variables during stress may be different during acute and chronic stressors. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

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. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Acute Stressors and Cortisol Responses: A Theoretical Integration and Synthesis of Laboratory Research.

This meta-analysis reviews 208 laboratory studies of acute psychological stressors and tests a theoretical model delineating conditions capable of eliciting cortisol responses. Psychological stressors increased cortisol levels; however, effects varied widely across tasks. Consistent with the theoretical model, motivated performance tasks elicited cortisol responses if they were uncontrollable or characterized by social-evaluative threat (task performance could be negatively judged by others), when methodological factors and other stressor characteristics were controlled for. Tasks containing both uncontrollable and social-evaluative elements were associated with the largest cortisol and adrenocorticotropin hormone changes and the longest times to recovery. These findings are consistent with the animal literature on the physiological effects of uncontrollable social threat and contradict the belief that cortisol is responsive to all types of stressors. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sympathetic reactivity to acute stress and immune response in women

We evaluated if the effects of acute stress on immune parameters were apparent in only the women who showed concomitant and substantial sympathetic nervous system activation and after statistical adjustment for changes in plasma volume. Nineteen women in the follicular stage of their menstrual cycles were assessed for immunological responsiveness to a series of three 3-minute psychological tasks, which reliably elicit cardiovascular and neuroendocrine stress responses. Women were classified as high or low sympathetic reactors based on their cardiovascular and neuroendocrine responses to one of the three tasks, a public speaking task. The stress-induced decreases in CD4+ percentage and increases in natural killer cell number and cytolytic activity were only apparent among the high reactors. Further analysis adjusting for alterations in plasma volume changes showed that the increase in NK cell number remained. Stress-induced proliferative responses to pokeweed mitogen and phytohemagglutinin were not more apparent among high reactors. These results are consistent with the hypothesis that the sympathetic nervous system plays a direct role in modulating the short term response to stress of some indices of the immune system in women.     

Stress, appraisal, coping, and social support as predictors of adaptational outcome among dementia caregivers.

A stress and coping model was used to study predictors of individual differences in caregiver adaptation. A total of 54 family caregivers of elderly dementia patients completed interviews and questionnaires assessing the severity of patient impairment and caregiving stressors; caregiver appraisals, coping responses, and social support and activity; and caregiver outcomes, including depression, life satisfaction, and self-rated health. Correlational and regression analyses supported the utility of the stress and coping model. Appraisal, coping responses, and social support and activity were significant predictors of caregiver outcome, even when severity of caregiving stressors was statistically controlled. The importance of a multidimensional approach to assessing caregiver outcomes was supported by regression analyses indicating that each caregiver outcome was predicted by different patterns of stressors, appraisal, coping, and social support and activity. Results are discussed in terms of a stress and coping model of caregiving, and clinical implications for work with caregiving families. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The influence of the great Hanshin earthquake on human response to environmental vibration due to the Shinkansen

OBJECTIVE: To describe the relationships between cardiovascular and natural killer (NK) cell number changes on acute psychological stress in women. METHOD: Data from eight different studies were analyzed. A total of 128 healthy female subjects, 85 younger (18-45 years) and 43 older (49-87 years), had been subjected to a speech stressor (N = 80) or a mental effort stressor (N = 48), mental arithmetic, or the Stroop test. Correlations between changes in NK cell numbers, systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were computed. Meta-analysis programs were used to study correlations across studies and to examine whether correlations differed with stressors or age. RESULTS: In all studies, significant increases over baseline were observed for each variable. Across studies, the mean weighted r between changes in HR, DBP, and SBP was medium (rw = .25) to large (rw = .64). A medium to large average correlation between HR and NK changes (rw = .37) was observed, whereas average correlations of changes in NK cell numbers with blood pressure changes were small to medium (rw < or = .23). Correlations between changes in NK cell numbers and cardiovascular variables were homogeneous across studies, whereas mutual correlations between cardiovascular variables were heterogeneous. One moderator variable showed itself: correlations between HR and DBP reactions were larger in studies with older than younger subjects. CONCLUSION: NK cell changes and HR responses induced by acute stress in women are regulated, to some extent, by the same mechanisms. Neither the type of stressor nor age seem to be very important when considering correlations between NK cell and cardiovascular changes. This study integrates information about NK cell and cardiovascular responses in women that can be used as reference material in future studies.     

Aging and immune response to exercise

Human immune function undergoes adverse changes with aging. The T cells, which have a central role in cellular immunity, show the largest age-related differences in distribution and function, with thymus involution as the apparent underlying cause. The immune responses to acute exercise and training have not been studied extensively in the elderly. The natural killer (NK) cell response to a single exercise challenge is normal in older individuals, but immediately after exercise the elderly subjects manifest less suppression of phytohemagglutinin (PHA)-induced lymphocyte proliferation than younger individuals. In contrast, a strenuous exercise seems to induce a more sustained postexercise suppression of cellular immunity in older individuals than in their young peers. A few cross-sectional comparisons of immune status between physically fit elderly individuals and young sedentary controls suggest that habitual physical activity may enhance NK cell activity, checking certain aspects of the age-related decline in T cell function, such as reduced mitogenesis in response to plant lectins and decreases in the production of certain types of cytokine. The clinical implications, however, remain to be clarified by future study.     

Time-dependent differential changes of immune function in rats exposed to chronic intermittent noise

Noise is a highly relevant environmental and clinical stressor. Compared to most other experimental stressors, noise is a modest activator of neuroendocrine pathways that mimic the situation in human health where neuroendocrine activation by environmental stressors is often absent or difficult to establish. Little is known about the effects of noise exposure on the immune system. In the present work, the effects of a low-intensity chronic intermittent unpredictable noise regimen on various parameters of immune function was studied. Male wistar rats were exposed to a randomized noise protocol (white noise, 85 dB, 2-20 kHz) for 10 h per day, 15 min per h over a total period of 3 weeks. Control animals were exposed to ambient sound only. Immune function was monitored after 24 h, 7 days, and 21 days of noise exposure. Noise induced several significant changes in immune function in a time-dependent differential pattern involving both immunosuppression and immunoenhancement. After 24 h, serum IgM levels were increased and peripheral phagocytic activity was decreased. Splenic lymphocytic proliferation to mitogens was significantly decreased after 7 days, but slightly elevated after 3 weeks. The activity of splenic NK cells was increased significantly after 24 h and 7 days, but suppressed after 3 weeks. These results show that various parameters of immune function are affected differentially over time in a period of chronic mild noise stress, possibly due to sequential activation of different physiological mechanisms.     

Intermittent but not continuous inescapable footshock stress and intracerebroventricular interleukin-1 similarly affect immune responses and immunocyte beta-endorphin concentrations in the rat

Both CNS- and immunocyte(lymphocytes, splenocytes)-derived beta-endorphin is involved in immune responses to stress. We show in the rat that stress-induced immunodepression (decrease of mitogen-induced lymphocyte proliferation and NK activity) is present only after the administration of a stress paradigm that increases immunocyte-derived beta-endorphin, while this is absent when the concentrations of the opioid are not modified. Interestingly, plasma corticosterone levels were similarly elevated after stresses whether or not they suppress immune responses, thus suggesting a pivotal role of the opioid. The increase of immunocyte beta-endorphin and immunosuppression are similarly present also after the intracerebroventricular administration of interleukin 1, thus suggesting a role for this cytokine in stress responses. The modifications of immunocyte beta-endorphin concentrations and immune responses induced by stress and interleukin 1 are not affected by indomethacin, adrenalectomy or hypophysectomy, whereas they are completely blocked by a CRH antagonist and depletion of the serotoninergic or catecholaminergic systems. In conclusion, our results suggest that immune responses to stress are not uniquely linked to an activation of the HPA axis.     

Stress-induced suppression of natural killer cell cytotoxicity in the rat: A naltrexone-insensitive paradigm.

The suppression of natural killer (NK) cell cytotoxicity by footshock stress can be attenuated by opioid antagonists, implicating endogenous opioids in its mediation. A stress paradigm that includes NK suppression that is not blocked by the opioid antagonist naltrexone is reported. This stress paradigm is also shown to cause analgesia and elevated plasma corticosterone levels that are not attenuated by naltrexone. In the first experiment, a significant suppression of NK cell cytotoxicity after forced swimming was demonstrated in Fischer 344 rats treated with either saline or naltrexone, compared with nonstressed controls. Significantly higher corticosterone levels were evident in both stressed groups. In the second experiment, the same stress paradigm was shown to cause significant analgesia in the tail-flick test. It is concluded that opioids need not always be involved in the suppression of NK cell cytotoxicity by stress. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Enhancing versus suppressive effects of stress hormones on skin immune function

Delayed-type hypersensitivity (DTH) reactions are antigen-specific cell-mediated immune responses that, depending on the antigen, mediate beneficial (e.g., resistance to viruses, bacteria, and fungi) or harmful (e.g., allergic dermatitis and autoimmunity) aspects of immune function. Contrary to the idea that stress suppresses immunity, we have reported that short-duration stressors significantly enhance skin DTH and that a stress-induced trafficking of leukocytes to the skin may mediate this immunoenhancement. Here, we identify the hormonal mediators of a stress-induced enhancement of skin immunity. Adrenalectomy, which eliminates the glucocorticoid and epinephrine stress response, eliminated the stress-induced enhancement of skin DTH. Low-dose corticosterone or epinephrine administration significantly enhanced skin DTH and produced a significant increase in the number of T cells in lymph nodes draining the site of the DTH reaction. In contrast, high-dose corticosterone, chronic corticosterone, or low-dose dexamethasone administration significantly suppressed skin DTH. These results suggest a role for adrenal stress hormones as endogenous immunoenhancing agents. These results also show that hormones released during an acute stress response may help prepare the immune system for potential challenges (e.g., wounding or infection) for which stress perception by the brain may serve as an early warning signal.     

Diagnostic value of Western blotting in carbohydrate-deficient glycoprotein syndrome

Cytomegalovirus (CMV) infection has been associated with graft rejection in solid organ transplantation and with graft-versus-host disease in marrow transplantation. We hypothesized that CMV-infected endothelial cells play an important role in the rejection process, because of their strategic localization at the interface with the host immune system and their ability to modulate T cell function. To study the effect of CMV infection on cell-mediated cytotoxicity against endothelial cells, peripheral blood mononuclear cells (MNC) were incubated with CMV-infected umbilical vein endothelial cells (CMV-UVEC) or mock-infected controls (M-UVEC) and lysis measured by [3H]leucine release. MNC lysed only CMV-UVEC to a maximum of 23% at E:T 20:1. Lysis was not affected by CD3+ cell depletion, but was abolished by CD16+ cell depletion, indicating that NK cells were the effectors. The kinetics of the NK-mediated lysis of CMV-UVEC paralleled the time course of CMV antigen expression. Furthermore, ganciclovir treatment of CMV-UVEC cultures decreased both specific antigen synthesis and NK-mediated lysis. This indicated that NK might recognize either a viral antigen or a cellular antigen modulated by CMV infection. Treatment of CMV-UVEC with F(ab)2 fragments of human polyclonal anti-CMV antibodies failed to inhibit NK cytotoxicity. In contrast, F(ab)2 fragments of MB40.5, a murine MAb reactive with a conserved epitope on the human MHC class I, significantly decreased lysis, proving that NK lysis of CMV-UVEC is an MHC class I-dependent function. To determine whether CMV-UVEC lysis was dependent solely on upregulation of MHC class I, MNC were incubated with CMV-UVEC mixed with uninfected UVEC. There was no competition for NK-target recognition sites, indicating that NK lysis required an interaction with an MHC class I antigen modified by viral infection. Antibodies against IFN-alpha or -beta did not block NK cytotoxicity against CMV-UVEC. Our findings provide a working frame for further evaluation of cellular immune responses to CMV infection.     

Caregiving outcomes for older mothers of adults with mental retardation: A test of the two-factor model of psychological well-being.

A two-factor model of caregiving appraisal and psychological well-being, based on previous findings with caregiving spouses (M. P. Lawton et al; see record 1991-34214-001) was tested with 225 older mothers who provided care at home to an offspring with mental retardation The effects of objective caregiving stressors, caregiver resources, and subjective appraisals (caregiving satisfaction and burden) on the positive and negative dimensions of psychological well-being were examined. LISREL 8 analyses revealed that the model differed in two key ways for caregiving mothers: (a) Positive psychological well-being appeared to diminish subjective burden, and (b) both objective stressors and resources were unrelated to subjective burden. These findings suggest the need for future research into how caregiving dynamics are influenced by the specific nature of the relationship between the caregiver and the recipient. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Role of NK cells in early host response to chlamydial genital infection

The cell-mediated immune response has been documented to be the major protective immune mechanism in mice infected genitally with the agent of mouse pneumonitis (MoPn), a biovar of Chlamydia trachomatis. Moreover, there is strong evidence to indicate that gamma interferon (IFN-gamma) is a major effector mechanism of the cell-mediated immune response. Previous studies from this laboratory have also reported that the dominant cell population in the genital tract is the CD4 Th1 population. When experiments were performed by the enzyme-linked immunospot assay, high numbers of cells producing IFN-gamma were found in the genital tract, concomitant with resolution of the infection; however, in addition, an increase in IFN-gamma-producing cells which were CD4(-) was seen early in the infection. Since natural killer (NK) cells produce IFN-gamma and have been found to participate in the early responses in other infections, we hypothesized that NK cells are responsible for early IFN-gamma production in the murine chlamydial model. NK cells were quantified by the standard YAC-1 cytotoxicity assay and were found to appear in the genital tract as early as 12 h after intravaginal infection with MoPn. The cells were confirmed to be NK cells by abrogation of YAC-1 cell cytotoxicity by treatment in vitro and in vivo with anti-asialo-GM1. The early IFN-gamma response could also be depleted by treatment with anti-asialo-GM1, indicating that NK cells were responsible for the production of this cytokine. Of interest was our observation that depletion of NK cells also exacerbated the course of infection in the mice and elicited a Th2 response, as indicated by a marked increase in immunoglobulin G1 antibody. Thus, these data demonstrate that NK cells are not only responsible for the production of IFN-gamma early in the course of chlamydial genital tract infection but are also, via IFN-gamma, a significant factor in the development of the Th1 CD4 response and in the control of the infection.     

Individual differences in cardiac sympathetic control predict endocrine and immune responses to acute psychological stress.

Potential mechanisms coordinating individual differences in cardiovascular reactivity and endocrine and immune responses to acute psychological stress were examined. 23 young, healthy women performed a mental arithmetic challenge while measures of cardiovascular, endocrine, and immune function were assessed. Results revealed that the acute stressor was associated with changes in the cardiovascular, endocrine, and immune systems. More important, analyses revealed that individual differences in cardiovascular reactivity predicted stress-induced cortisol changes. Furthermore, cardiac sympathetic control, as indexed by preejection period, was specifically related to changes in natural killer cell activity. These results suggest that distinct physiological pathways are activated in response to acute psychological stress. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Immune changes induced by exercise in an adverse environment

Both physical activity and exposure to environmental stressors such as cold, heat, and high altitudes modify various components of immune function: T cell counts, natural killer (NK) cell counts, and cytolytic activity, cytokine secretion, lymphocyte proliferation and immunoglobulin levels. Light physical activity or a moderate level of environmental stress stimulate the immune response, but exhausting physical activity or more severe environmental stress have a suppressant effect, manifested by a temporary increase in susceptibility to viral infections. Combinations of physical activity and environmental stress generally have at least an additive effect. Thus, an intensity of physical activity or of environmental stress that is beneficial in itself can readily cause immunosuppression if the body is challenged by the two stimuli simultaneously.     

The relationship between cardiac reactivity in the laboratory and in real life.

Objective: An excessive cardiovascular response to acute stress is a probable risk factor for cardiovascular (CV) disease. Such reactivity is usually assessed from the CV response to laboratory stressors. However, if it is a risk factor, correlated responses must occur in real life. Design: In the present study, we investigated the relationship between the heart rate (HR) response to five laboratory stressors and HR reactivity in the field. Measures: HR variation, the response to a real life stressor (public speaking), and the increase in HR with periods of self-reported tense arousal. Ambulatory HR, activity and posture were measured continuously over a 7-hr period. Results: The HR increase to laboratory stressors did not relate to HR variation consistently, but it did relate to the other two field measures. Conclusion: The results suggested that a tendency to increased HR reactivity may be a risk factor for cardiovascular disease when combined with exposure to stress. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Chronic stress influences cardiovascular and neuroendocrine responses during acute stress and recovery, especially in men.

This study tests the influence of chronic stress on cardiovascular and neuroendocrine responses to and recovery from acute stressors and whether the effects are gender specific. Sixty-two healthy, middle-aged persons (50% women) performed mental-arithmetic and public-speaking tasks and relaxed thereafter for 1 hr while their cardiovascular and neuroendocrine functions were measured. Participants with higher levels of chronic stress showed lower systolic blood pressure (SBP) and epinephrine (E; men only) and marginally lower levels of norepinephrine (NE) responses to the tasks and showed lower levels of cortisol and marginally lower NE responses during recovery. Relative to women, men had high diastolic blood pressure (DBP) responses to the tasks and high SBP, DBP, and E responses during recovery. Gender differences in cardiovascular disease in midlife may be due to gender differences in inability to recover quickly, in addition to enhanced acute-stress response. (PsycINFO Database Record (c) 2010 APA, all rights reserved)