Psychological Stress Increases Human T Cell Apoptosis in vitro

Sakami, Shotaro; Nakata, Akinori; Yamamura, Takashi; Kawamura, Noriyuki

doi:10.1159/000068326

Cited by 13 publications

(8 citation statements)

References 28 publications

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“…Similar to our findings, apoptosis has previously also been shown in a variety of immune cells under physiological or pathological conditions, such as activation-induced apoptosis in peripheral T cells, mediated through Fas-Fas ligand interaction, [13] or accelerated spontaneous apoptosis in CD4+ T cells in depressed patients [48] . Moreover, previous in vitro studies demonstrated that T cell depletion after psychological stress occurs by apoptosis in accordance with our findings [49] .…”

Section: Discussionsupporting

confidence: 93%

Effect of Gender and Menstrual Cycle on Immune System Response to Acute Mental Stress: Apoptosis as a Mediator

Pehlivanoğlu

Bayrak

Gurel

et al. 2011

Neuroimmunomodulation

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Background/Aims: We aimed to explore the immunological outcomes of short-term mental stress in apoptosis in peripheral lymphocytes and variations by gender and hormonal status of the individuals together with possible mediators of this interaction. Methods: Acute mental stress (computerized Stroop color-word interference and cold pressor tests) was applied to men (n = 17) and women (n = 16, in both follicular and luteal phases). Heart rate and blood pressure were monitored throughout the test and after the test until baseline values were recorded. Blood samples were drawn for measuring cortisol and nitric oxide (NO) levels and flow-cytometric cell counting before and after the test. Results: Activation of the stress system was ascertained by increased heart rate, blood pressure and serum cortisol levels after the test. Relative to baseline values, acute mental stress altered the distribution of T and natural killer cells. There was a significant decrease in T helper/T cytotoxic-suppressor cell ratio and an increase in apoptotic T helper cell percentage irrespective of gender or menstrual cycle phase. An increased number of natural killer cells was detected in women, whereas it was decreased in men. After stress induction, serum NO levels remained the same in women and increased in men. Although a correlation was not found between immune system changes and NO levels, glucocorticoids seem to have a role in the observed differences. Conclusion: Acute mental stress triggers apoptotic T helper cell loss which was associated with stress system activation, and sex steroids affect the pattern of stress-related immune cell distribution.

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Section: Discussionsupporting

confidence: 93%

Effect of Gender and Menstrual Cycle on Immune System Response to Acute Mental Stress: Apoptosis as a Mediator

Pehlivanoğlu

Bayrak

Gurel

et al. 2011

Neuroimmunomodulation

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“…Moreover, the observed partial mediating effect of stress neuropeptides in the association between pain ratings and lymphocyte Fas expression is consistent with previous evidence implicating stress in the modulation of apoptosis and activation of the JNK pathway 35. Psychological stress36 and stress hormones37 have been reported to induce lymphocyte apoptosis in humans and in animal models 38. Based on the above, the role of stress peptides in the regulation of pain-related apoptosis merits to be investigated further.…”

Section: Discussionsupporting

confidence: 88%

Association between lymphocyte expression of the apoptotic receptor Fas and pain in critically ill patients

Papathanassoglou

Mpouzika

Giannakopoulou

et al. 2017

JPR

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ObjectiveLymphocyte apoptosis in critical illness is associated with immunosuppression. We explored for the first time the associations between pain ratings and expression of the apoptotic receptor Fas on B and T cells in critically ill patients and the potential mediating effects of adrenocorticotropic hormone (ACTH), cortisol, and substance P (SP).DesignThis is an exploratory correlational study with repeated measurements (14 days followup) and cross-sectional comparisons.SettingThis study was conducted in a state hospital in the metropolitan area of Athens, Greece.ParticipantsThe participants were 36 consecutive critically ill patients and 36 matched controls.Outcome measuresPain measured by the self-reported numeric rating scale [NRS], the behavioral pain scale, and the pain assessment scale was the primary outcome measure. Flow cytometry (Fas), electrochemiluminescence (ACTH and cortisol) and enzyme-linked immunosorbent assay (SP) were used. Mixed linear models for repeated measurements and bivariable associations at discrete time points were employed.ResultsSignificant pain at rest was noted. Pain ratings associated with Fas expression on cytotoxic T cells (P=0.041) and B cells (P=0.005), even after adjustment for a number of clinical treatment factors (P=0.006 and P=0.052, respectively). On the day that more patients were able to communicate, Fas on B cells (r=0.897, P=0.029) and cytotoxic T cells (r=0.832; P=0.037) associated with NRS ratings. Associations between pain ratings and ACTH serum levels were noted (P<0.05). When stress neuropeptide levels were added to the model, the statistical significance of the associations between pain ratings and Fas expression was attenuated (P=0.052–0.063), suggesting that stress neuropeptides may partially mediate the association.ConclusionPreliminary evidence for the association between pain and lymphocyte apoptotic susceptibility is provided. The role of pain management in maintaining immunocompetence in critical illness is worth exploring.

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“…Interestingly, flow cytometric assessments have revealed that CD4+ T cells from depressed patients exhibit evidence of accelerated spontaneous apoptosis as well as increased expression of the receptor for Fas (CD95), which mediates apoptotic signaling by Fas-ligand (Eilat et al, 1999; Ivanova et al, 2007; Szuster-Ciesielska et al, 2008). Increased T cell apoptosis has also been observed as a function of chronic stress in both humans and laboratory animals (Sakami et al, 2002; Shi et al, 2003). One possibility that might explain increased T cell apoptosis in depression, especially in the context of increased immune activation, is tryptophan depletion.…”

Section: T Cells and Depressionmentioning

confidence: 99%

Depression and immunity: A role for T cells?

Miller

2010

Brain, Behavior, and Immunity

280

187

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Much attention has been paid to the potential role of the immune system in the pathophysiology of major depression in humans. While activation of innate immune responses currently dominates the research landscape, early studies in depressed patients demonstrating impairment in acquired immune responses, in particular T cell responses, may warrant further consideration. Intriguing data suggest that activated T cells may play an important neuroprotective role in the context of both stress and inflammation. For example, generation of autoreactive T cells through immunization with central nervous system (CNS) specific antigens has been shown to reverse stress-induced decreases in hippocampal neurogenesis as well as depressive-like behavior in rodents. In addition, trafficking of T cells to the brain following stress, in part related to glucocorticoids, has been found to reduce stressinduced anxiety-like behavior. Data indicate that T regulatory cells may also play a role in depression through downregulation of chronic inflammatory responses. Based on the notion that T cells may subserve neuroprotective and anti-inflammatory functions during stress and inflammation, impaired T cell function may directly contribute to the development of depression. Indeed, increased sensitivity to apoptosis as well as reduced responsiveness to glucocorticoids, may not only decrease the availability of T cells in depressed patients, but also may reduce their capacity to traffic to the brain in response to relevant neuroendocrine or immune stimuli. Further elucidation of T cell pathology may lead to new insights into immune system contributions to depression. Moreover, enhancement of T cell function may represent an alternative strategy to treat depression.

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Psychological Stress Increases Human T Cell Apoptosis in vitro

Cited by 13 publications

References 28 publications

Effect of Gender and Menstrual Cycle on Immune System Response to Acute Mental Stress: Apoptosis as a Mediator

Effect of Gender and Menstrual Cycle on Immune System Response to Acute Mental Stress: Apoptosis as a Mediator

Association between lymphocyte expression of the apoptotic receptor Fas and pain in critically ill patients

Depression and immunity: A role for T cells?

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