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

This study examined enumerative immune and catecholamine measures and their response to a speaking stressor in 20 healthy women during two phases of the menstrual cycle. Subjects were studied at the same time of day on two separate occasions approximately 6 weeks apart, once during the follicular phase (Days 7-10 following menses) and once during the luteal phase (Days 7-10 following the LH surge) of the cycle. The stressor was associated with significantly increased CD8 cells (p < .001). NK cells (CD16, CD56, and CD57, p < .001), and plasma norepinephrine (p < .01) and decreased CD4/CD8 ratio (p < .001). There were no significant main effects for menstrual phase nor significant interactions for menstrual phase by task for any dependent variable. Baseline and stress test-retest correlation coefficients were similar to those reported in the literature for men and indicate a moderate test-retest reliability. Change score test-retest correlation coefficients were consistently smaller and only CD56 (r = .49) and the CD4/CD8 ratio (r = .55) correlated significantly. The findings suggest that the changes in reproductive hormones associated with the menstrual cycle have no appreciable effect on lymphocyte numbers or their response to acute stress. Given estrogen's long-term duration of action, it may be that their menstrual cycle does not afford an adequate window of time to scrutinize reproductive hormone effects on the immune functioning.
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PMID:Enumerative immune changes following acute stress: effect of the menstrual cycle. 859 Aug 16

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

Clinical observations suggest that psychological stress induces exacerbation of disease activity in patients with systemic lupus erythematosus (SLE). In order to determine whether SLE patients differ from healthy controls in their stress response, we analyzed heart rate, blood pressure, catecholamine concentration, lymphocyte subpopulations, natural killer (NK) cell activity, and expression of beta-adrenoceptors on PBMC before, immediately after, and 1 h after a public speaking task in 15 SLE patients and 15 healthy subjects. Both groups demonstrated similar psychological, cardiovascular, and neuroendocrine responses to acute stress. However, natural killer (CD16(+)/CD56(+)) cell numbers transiently increased after stress exposure, with significantly less pronounced changes in SLE patients. In addition, NK activity increased in healthy controls (n = 8) but not in SLE patients (n = 4) after acute stress. Furthermore, the number of beta(2)-adrenoceptors on PBMC significantly increased only in healthy subjects (n = 8) after stress but not in SLE patients (n = 7). These data indicate that SLE patients differ from healthy controls in stress-induced immune responses.
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PMID:Patients with systemic lupus erythematosus differ from healthy controls in their immunological response to acute psychological stress. 1060 Feb 17

Psoriasis (PSO) is a mainly T helper-type 1 (TH(1)) cell mediated chronic inflammatory skin disease characterized by epidermal hyperproliferation and psoriatic plaques. There is ample evidence that stress may trigger psoriatic eruption, however, the underlying mechanisms of stress-induced exacerbation of PSO are poorly understood. The specific goal of the present study was to investigate the impact of acute stress on pathologically relevant immune functions in PSO patients. PSO patients (n=23) and healthy controls (n=25) were exposed to a standardized laboratory stressor ("Trier Social Stress Test", TSST) including a free speech and mental arithmetics in front of an audience. Blood samples were collected 10min before and 1, 10, 20, and 60min after the TSST as well as 24h after the experiment at identical time points under resting conditions. Analyses of leukocyte subsets indicated a significantly increased number of leukocyte subpopulations (lymphocytes, granulocytes, CD3(+), CD8(+), CD16(+)/CD56(+), and CD3(+)/HLA-DR(+)) after the TSST (all p<.01) with no significant between-group differences. However, monocyte number (F(3,120)=2.7; p<.01) and number of CD4(+)cells (F(3,120)=3.09; p<.05) were found to be significantly higher in PSO sufferers than in controls. Moreover, a significant decrease of CD3(+)/CD25(+)cells was observed in the PSO, but not in the control group (F(3,120)=3.46; p<.05). After exposure to the TSST, stimulation of peripheral blood mononuclear cells (PBMCs) with phytohemagglutinin (PHA) resulted in elevated production of IFN-gamma (F(3,126)=6.9; p<.001) and IL-2 (F(3,123)=6.6; p<.001), and moreover, a decreased production of IL-10 (F(3,132)=5.22; p<.01) and IL-4 (F(3,129)=3.9; p<.01). No difference in stress-induced changes of cytokine production to PHA could be identified between the two experimental groups (all p>.05). The present findings suggest that acute psychosocial stress is associated with changes of immune functions known to be involved in PSO which may be one potential explanation of how stress may trigger psoriatic eruption.
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PMID:Altered distribution of leukocyte subsets and cytokine production in response to acute psychosocial stress in patients with psoriasis vulgaris. 1671 97

It is well-known that acute stress, presumably as a first defense against pathogens, enhances PBMC counts by mobilizing these beta2-adrenoceptor positive cells from the marginal pool. Yet, only select leukocyte subsets participate in this phenomenon of adrenergic leukocytosis and underlying mechanisms are obscure. In this study, we analyzed in human blood adhesion molecule and chemokine receptor profiles in 14 leukocyte subsets, and responsiveness of subsets to epinephrine in vivo and in vitro. Five subsets, namely, CCR7(-)CD45RA(+)CD8(+) effector T cells, CD4(-)CD8(-) gamma/delta T cells, CD3(+)CD56(+) NKT-like cells, CD16(+)CD56(dim) cytotoxic NK cells, and CD14(dim)CD16(+) proinflammatory monocytes showed a rapid and transient increase after infusion of epinephrine at physiological concentrations. These cells were characterized by a CD62L(-)CD11a(bright)CX3CR(bright) phenotype, whereby expression of both CD11a and CX3CR1 was strongly correlated with adrenergic leukocytosis in vivo (r = 0.86 and 0.78, p < 0.005). The same subsets showed highest adherence to activated endothelium in vitro, which (except for proinflammatory monocytes) was reversed by epinephrine. We conclude that these five cytotoxic effector leukocyte subsets comprise the marginal pool by a CD11a/CX3CR1-mediated attachment to the endothelium. Epinephrine rapidly attenuates this attachment to allow demargination and release of the cells into the circulation that, because of their cytotoxic effector function, provide immediate protection from invading pathogens.
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PMID:Selective mobilization of cytotoxic leukocytes by epinephrine. 1994 13