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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several investigators have demonstrated that immune responses may be subject to classical conditioning processes. Conditioning effects in both cell-mediated and humoral immune responses have been reported. Strong evidence for behavioral effects on immune responses has been provided by studies of stress-induced immunosuppression. Stressors may increase morbidity due to infectious agents, depress antibody responses, inhibit lymphocyte reactions, and attenuate several other cell-mediated immune functions. In our studies, acute inescapable footshock inhibited natural killer cell (NK) activity in CD-1 and C57BL/6J mice, but not in DBA/2J mice. Genetic factors play a role in the immunological responses to stress. In contrast to the effects of acute stress, NK activity of mice exposed to chronic inescapable footshock was not reduced from control levels. Adaptive processes may be invoked during repeated stress exposure, thereby limiting the potentially damaging effects of the stressor.
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PMID:Behavioral influences on the immune system: stress and conditioning. 349 85

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.
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PMID:Sympathetic reactivity to acute stress and immune response in women. 860 Apr 83

This study examined relationships between psychologic characteristics and enumerative immune responses to an acute laboratory stressor. Lymphocyte subsets were measured in 104 subjects at rest and following a 6-minute laboratory naturalistic speaking stressor. Multiple linear regression was utilized to assess relationships between immune reactivity (change scores) and anger expression, hostility, anxiety, depression, and stress. The task resulted in significant increases over baseline in WBC (p < 0.001), T-suppressor/cytotoxic CD8 cells (p = 0.010) natural killer CD56 cells (p < 0.0001), and CD57 (p < 0.0001) cells, and significant decreases in T-cells (p = 0.012), T-helper cells (p = 0.003), B-cells (p < 0.001), and the T-helper/suppressor ratio (p < 0.001). In general, the regression suggested that moderate associations exist between certain psychologic attributes and acute subset redistribution. For example, the increase in natural killer cell subsets was significantly negatively associated with anger expression, hostility, and depression. Suppressor/cytotoxic (CD8) cell reactivity was associated with baseline as well as with the task-induced changes in anxiety. B-cell (CD19) responses were related to the subject's age, expression of anger, and depression scores. As with the cardiovascular reactivity literature, these findings suggest that a relationship exists between certain psychologic characteristics such as anger and anxiety and immune reactivity to acute stress.
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PMID:Psychologic characteristics associated with acute stressor-induced leukocyte subset redistribution. 873 22

Weanling pigs (n = 132) were used to investigate the effects of three common stressors (and a control) and differing social status on behavior, immunity, plasma cortisol, blood chemical, and performance measures. Eleven blocks of 12 pigs each were evaluated. Each pen contained three pigs of dominant (DOM), intermediate (INT), or submissive (SUB) social status. Two weeks later, random pens of pigs experienced either a control treatment (CON) or they were stressed for 4 h by shipping (SHIP), heat-stressed (HEAT) with overhead heat lamps in their home pens, or cold-stressed (COLD) by direct application of water and an air current. Treatments did not influence body weights; however, percentage weight loss during SHIP was greater than for other treatments. Body weights were heavier for DOM pigs than for INT and SUB pigs. Social status had large effects on plasma cortisol, globulin, acute-phase proteins, body weight, and weight changes. Only acute shipping stress resulted in weight loss. Many immune and blood measures were not changed among acutely stressed pigs; however, the relationship between social status and mitogen-induced lymphocyte proliferation and natural killer cell cytotoxicity was disrupted during acute stress. Pig behavior was significantly changed by each stress treatment in a unique manner. During acute stress, behavioral changes seem to be the most consistent and reliable indicators.
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PMID:Behavioral, endocrine, immune, and performance measures for pigs exposed to acute stress. 949 55

Acute mental and physical stress lead to a marked lymphocytosis, with circulating natural killer cell numbers showing the most prominent increase. Many studies have linked these acute stress effects on lymphocytes with an increase in catecholamine levels. However, the molecular mechanisms which mediate this redistribution of lymphocytes from lymphocyte reservoirs into the circulation remain unknown. We hypothesized that this form of lymphocytosis was in part due to shedding of cell adhesion molecules from the cell surface and a subsequent detachment of lymphocytes adhering to the vascular endothelium in lymphocyte reservoirs. In this study, healthy human volunteers (n = 12) were exercised on a treadmill until exhaustion. The circulating levels of the soluble cell adhesion molecules ICAM-1 and E-Selectin were determined by ELISA. The subjects were then randomly assigned to treatment with either propranolol or metoprolol and repeated the exercise protocol after 1 week of treatment. Prior to drug treatment, soluble ICAM-1 levels rose from 258 +/- 19 to 321 +/- 28 ng/ml following exercise and returned to approximate baseline levels of 263 +/- 22 ng/ml after 1 h of rest. This highly significant effect of exercise on circulating ICAM-1 levels (p < .005) was mitigated after treatment with the beta-adrenergic antagonists. Soluble E-Selectin levels were not significantly affected by exercise. These results suggest that dynamic exercise leads to shedding of the cell adhesion molecule ICAM-1 via adrenergic mechanisms. We believe that these findings will contribute to the understanding of how physical and mental stress modulate lymphocyte migration and adhesion.
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PMID:Dynamic exercise leads to an increase in circulating ICAM-1: further evidence for adrenergic modulation of cell adhesion. 951 20

The present study explored cardiovascular and immune responses to a standardized laboratory challenge (speech task) in 23 breast cancer patients. All patients were diagnosed with positive axilliary lymph nodes and received tamoxifen as an adjuvant treatment throughout the course of the study. As a control group, 15 age-matched healthy women were included. At baseline, there were no differences in blood pressure and heart rate values between breast cancer patients and healthy women. With respect to the lymphocyte subsets at baseline, patients had significantly higher absolute numbers of CD16/56 (NK) cells. We speculate that the increase in circulating NK cells can be either a sign of activation of aspecific natural immunity caused by tumor cells or an immunostimulatory effect of tamoxifen. No differences were found in total lymphocyte count and numbers of CD3, CD4, CD8 or CD19 (B) cells. The pattern of changes induced by the speech task with regard to number and function of peripheral immune cells confirm earlier findings derived from healthy subjects. Overall, marked increases were observed in NK and CD8 cells, whereas smaller changes were observed in number of CD4 and CD19 (B) cells in response to the speech task. There were no significant differences in the acute stress-induced immune cell changes between breast cancer patients and healthy women. These results seem to implicate that the distribution of immune cells is intact in patients with localized breast disease. With respect to natural killer cell activity (NKCA), our results, as do those of others, show a significant increase in response to the speech task in both healthy women and patients. Compared to the NKCA responses of healthy women, those of breast cancer patients appeared to be delayed. Potential mechanisms behind this difference are discussed.
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PMID:Effect of mild acute stress on immune cell distribution and natural killer cell activity in breast cancer patients. 967 57

The purpose of this study was to determine the impact of locus of control, social support and their interaction on acute stress indicators as a consequence of the communication of the results of a breast biopsy. Immunological and psychological indicators were evaluated in 50 patients with breast tenderness. We found little evidence for the existence of a relationship between psychosocial variables considered to be stress indicators and acute stress symptoms. Concerning the results of the first assessment, only the relation between locus of control and psychological distress was meaningful. With regard to the existence of a relationship between psychosocial variables and natural killer cell system indicators, only the number of natural killer cells (NKC) could be explained by the psychosocial model including locus of control, perceived social support from relatives and the interaction between locus of control and perceived social support from relatives.
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PMID:Psychosocial predictors of psychological, neurochemical and immunological symptoms of acute stress among breast cancer patients. 1019 20

MDMA (3,4-methylenedioxymethamphetamine) use can cause neurochemical, behavioral and endocrine alterations, similar to those produced by exposure to acute stress, suggesting its potential as a "chemical stressor." It is known that stressful stimuli can produce a depression of immune function and an alteration in immune cells distribution. In vitro exposure to MDMA resulted in a modulation of several immune functional parameters such as T-cell regulatory function, cytotoxic T-lymphocyte activity, natural killer cell activity and macrophage function. Administration of MDMA in rats produced a rapid and sustained suppression of induced lymphocytes proliferation and a significant decrease in circulating lymphocytes. These alterations in rat immune function were accompanied by a significant rapid increase in plasma corticosterone concentrations. It was postulated that the result of altered induced proliferation response of lymphocytes could have been due to a combined effect of direct action of MDMA on lymphocytes and to the activation of the hypothalamic pituitary adrenal axis (HPA axis) and/or the sympathetic nervous system (SNS) via central mechanisms. In humans, acute MDMA treatment produced a time-dependent immune dysfunction associated with MDMA plasma concentrations. Although total leukocyte count remained unchanged, there was a decrease in CD4+ T-cells and functional responsiveness of lymphocytes to mitogenic stimulation, while percentage of natural killer cells significantly increased. A rise of cortisol plasma concentrations similar to that observed in the rat model supported the hypothesis of MDMA-induced release of corticotrophin-releasing factor from the median eminence of the hypothalamus and subsequent HPA axis and SNS activation. The present findings indicate that MDMA ingestion may represent a potential health hazard for an increased risk of immune system-related diseases.
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PMID:Immunomodulating activity of MDMA. 1108 23

Although acute stress has been reported to suppress natural killer cell activity (NKA) and host resistance to metastasis, it is unclear whether the sympathetic nervous system (SNS) has a role in these effects. The current study in Fischer 344 rats assessed the involvement of adrenal catecholamines and beta(1)- and beta(2)-adrenoceptors in mediating these deleterious effects of swim stress. In addition to assessing the number and activity of NK cells following swim stress, we used a tumor model based on the MADB106 mammary adenocarcinoma line: this syngeneic tumor metastasizes only to the lungs, and its lung tumor retention (LTR) and metastatic colonization are highly sensitive to NKA. The findings indicate that stress increased both LTR, assessed 24 h after inoculation, and the number of lung metastases, counted 3 weeks later. These effects were attenuated or completely abolished by the ganglionic blocker chlorisondamine (3 mg/kg i.p.), by adrenal demedullation, by a selective beta-adrenergic antagonist (nadolol, 0.4 mg/kg), and additively by a selective beta(1)- (atenolol, 1-6 mg/kg) and a selective beta(2)-antagonist (either butoxamine 4-32 mg/kg or ICI-118,551 0.3-8 mg/kg). Stress also suppressed NKA, and adrenal demedullation prevented this suppression. Administration of adrenaline (0.1-1 mg/kg) or of a beta-adrenergic agonist (metaproterenol, 0.8 mg/kg), in physiologically relevant doses, suppressed NKA in a dose-dependent manner, and increased LTR to levels characteristic of swim stress. Taken together, these findings suggest that acute stress, by releasing catecholamines from the adrenal glands and activating beta(1)- and beta(2)-adrenoceptors, suppresses NKA and consequently compromises resistance to NK-sensitive metastasis.
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PMID:Suppression of NK cell activity and of resistance to metastasis by stress: a role for adrenal catecholamines and beta-adrenoceptors. 1112 82

Recent research in rodents has demonstrated that exposure to bacterial endotoxin during the neonatal period alters the development of the hypothalamic-pituitary-adrenal axis resulting in hypersecretion of corticosterone after stress-exposure in adulthood. Given the known interactions between glucocorticoids and the immune system it was hypothesized that such alterations may impact on immune outcomes. Fischer 344 rats were treated with endotoxin (50 microg/kg Salmonella enteritidis, i.p.) or the vehicle on postpartum d 1, 3, 5, and 7. In adulthood, animals were subjected to chronic stress (6 x 10 h/d restraint stress), and the effect on resistance to tumor colonization (experiment 1) and natural killer cell activity (experiment 2) was assessed. Experiment 3 assessed corticosterone responses to acute stress in adulthood after neonatal endotoxin or saline treatment. Neonatal endotoxin exposure resulted in a 2-fold increase in tumor colonization (p < 0.001) and a significant impairment in the activity of natural killer cells (p < 0.01), cells critically involved in the surveillance and eradication of tumor cells. Neonatal endotoxin exposure also resulted in a significant decrease in gain weight that persisted into adulthood (p < 0.05), and potentiation of corticosterone responses to acute stress in adulthood (p < 0.05). We conclude that neonatal endotoxin exposure produces long-term changes in the hypothalamic-pituitary-adrenal axis, and has significant long-term effects on immune function, specifically in terms of resistance to tumor colonization in adulthood.
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PMID:Neonatal endotoxin exposure influences HPA responsivity and impairs tumor immunity in Fischer 344 rats in adulthood. 1172 35


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