Stable individual differences in physiological response to stressors: implications for stress-elicited changes in immune related health

Cohen, Sheldon; Hamrick, Natalie

doi:10.1016/s0889-1591(03)00110-7

Cited by 114 publications

(70 citation statements)

References 27 publications

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“…dACC is the dorsal anterior cingulate cortex; BA refers to putative Brodmann's area; MNI coordinates identify the local maxima of particular brain activations, reported in Montreal Neurological Institute (MNI) format; Cluster size (k) is the number of voxels in each activation cluster that was significantly associated with greater sTNFαRII responses to the TSST; t is the t-value at those coordinates (local maxima); r (TNF) is the correlation coefficient describing the strength of association between the activation cluster and sTNFαRII response to the TSST. ences in inflammatory responses to stress are relatively stable over time (29,30).…”

Section: Discussionmentioning

confidence: 99%

Neural sensitivity to social rejection is associated with inflammatory responses to social stress

Slavich

Way

Eisenberger

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

328

163

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Although stress-induced increases in inflammation have been implicated in several major disorders, including cardiovascular disease and depression, the neurocognitive pathways that underlie inflammatory responses to stress remain largely unknown. To examine these processes, we recruited 124 healthy young adult participants to complete a laboratory-based social stressor while markers of inflammatory activity were obtained from oral fluids. A subset of participants (n = 31) later completed an fMRI session in which their neural responses to social rejection were assessed. As predicted, exposure to the laboratory-based social stressor was associated with significant increases in two markers of inflammatory activity, namely a soluble receptor for tumor necrosis factor-α (sTNFαRII) and interleukin-6 (IL-6). In the neuroimaging subsample, greater increases in sTNFαRII (but not IL-6) were associated with greater activity in the dorsal anterior cingulate cortex and anterior insula, brain regions that have previously been associated with processing rejectionrelated distress and negative affect. These data thus elucidate a neurocognitive pathway that may be involved in potentiated inflammatory responses to acute social stress. As such, they have implications for understanding how social stressors may promote susceptibility to diseases with an inflammatory component.P sychological stress is intimately related to human health and well-being. It increases susceptibility to the common cold (1), elevates risk for several major diseases (2), and is a strong, independent predictor of morbidity and mortality. In a recent epidemiological study, for example, males experiencing high levels of stress were 32% more likely to die during a 22-y assessment period than were those experiencing low levels of stress (3).

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Section: Discussionmentioning

confidence: 99%

Neural sensitivity to social rejection is associated with inflammatory responses to social stress

Slavich

Way

Eisenberger

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

328

163

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“…Indicating the ability of leukocytes to produce a respiratory burst in response to in vitro Phorbol 12-myristate 13-acetate stimulation, following completion of the stressor protocol using Car A, was significantly reduced compared to the use of Car B. As qualitative data showed that subjects perceived completion of the protocol using Car A more psychologically stressful, the degree of physiological stimulation, through hypothalamic-pituitary-adrenal axis activity (Beuschlein et al, 2001;Cohen et al, 2003) resulted in a greater in vivo respiratory burst for treatment group A, leading to the observed reduced in vitro Phorbol 12-myristate 13-acetate stimulated respiratory burst.…”

Section: Discussionmentioning

confidence: 99%

Leukocyte responsiveness, a quantitative assay for subjective mental workload

Shelton-Rayner

Mian²,

Chandler

et al. 2012

International Journal of Industrial Ergonomics

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Assessing psychological stress and mental workload within work-based scenarios relies heavily upon qualitative, subjective, self-assessment techniques, many of which were originally intended for identifying specific pathological disorders and have reduced sensitivity when evaluating everyday stressors. Quantitative measures involve monitoring changes in the cardiopulmonary system and stress hormone concentration. Although these (e.g. heart rate and blood pressure) provide a basic, reactive indication of the presence of a psychological stressor, many are subject to influence by other bio-mechanisms, or are unable to provide rapid results due to complex laboratory analysis. This study demonstrates how immune responsiveness, known to be influenced by psychological stress, can be used to assess changes in mental workload. Healthy male and female subjects (aged between 26 and 55 years) provided capillary blood samples before and after completing the same, basic, driver-related tasks followed by a simple manoeuvre in two unfamiliar motor vehicles. Using a chemiluminescent technique termed Leukocyte Coping Capacity (LCC), the ability of leukocytes to produce reactive oxygen species in vitro was assessed. Significant post-stressor changes in leukocyte activity were demonstrated between treatment groups. These findings add weight to the proposition that leukocyte activation is a useful quantitative measure of psychological stress and mental loading in humans. This study demonstrates the diagnostic ability of LCC for use during ergonomic evaluation, however the potential industrial applications for this technique are numerous and diverse. KEY WORDSChemiluminescence; Ergonomics; Leukocytes; Mental Workload; Psychological Stress; Reactive Oxygen Species. 3 ABBREVIATIONSHmax-RLU adj , maximum control adjusted leukocyte activity; LCC, leukocyte coping capacity; RLU adj , control adjusted relative light units; T-max, time taken (minutes) to reach maximum control adjusted leukocyte activity; T=5, 10, and 15minutes, control adjusted leukocyte activity at 5, 10, and 15 minutes, respectively, into the 45 minute chemiluminescence sampling protocol. INTRODUCTIONEvaluation of psychological stress -a threat which would not require a physiological response which elicits physiological consequences (Segerstrom and Miller, 2004) relies heavily upon qualitative psychometric measures. Examples include: Present State Examination (Baker et al., 2003), the Brief Symptom Inventory (Brosig et al., 2007;Cuculi et al., 2006;Fellinger et al., 2007;Mansbach et al., 2005), and the BussDurkee Hostility Inventory (Bag et al., 2005). All were primarily designed to identify specific pathologic disorders, and validated using dysfunctional clinical populations with abnormal statistical distributions. Consequently these proved to have limited sensitivity when used to test below intended critical diagnostic thresholds (Lemyre and Tessier, 1988) -such as when investigating psychological and physiological transient laboratory stressors.As psychological...

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“…These stress-induced effects are not inconsequential; high stress reactivity has been linked to increased susceptibility to infection and immune dysfunction (Black, 2002;Padgett and Glaser, 2003;Glaser and Kiecolt-Glaser, 1998;Kiecolt-Glaser et al, 2002;Liu et al, 2002;Rohleder et al, 2001;Cohen and Hamrick, 2003). Some of these effects can be modeled on the laboratory, and as we and others have shown, social defeat activates the core stress responses and can have deleterious immunological effects on defeated mice (Devoino et al, 2003;Merlot et al, 2003;Padgett et al, 1998;Sheridan et al, 2000), including increased proinflammatory cytokine production, splenomegaly, trafficking of lymphocytes to the spleen, and insensitivity to the antiproliferative effects of glucocorticoids in LPS-stimulated splenocytes (Avitsur et al, 2003;Bailey et al, 2006;Engler et al, 2005;Stark et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Repeated social defeat causes increased anxiety-like behavior and alters splenocyte function in C57BL/6 and CD-1 mice

Kinsey

Bailey

Sheridan

et al. 2007

Brain, Behavior, and Immunity

167

133

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The experimental model, social disruption (SDR), is a model of social stress in which mice are repeatedly attacked and defeated in their home cage by an aggressive conspecific. In terms of the impact of this stressor on the immune response, SDR has been reported to cause hyperinflammation and glucocorticoid insensitivity. To this point however, the behavioral consequences of SDR have not been thoroughly characterized. Because social defeat has been reported to cause anxiety-and depressive-like behaviors, the current study was designed to assess whether SDR also causes anxietyand depressive-like behaviors. Using the light/dark preference test and the open field test as tools to measure behaviors characteristic of anxiety, the data showed that C57BL/6 and CD-1 male mice subjected to SDR displayed increased anxiety-like behavior. The increase in anxiety-like behaviors persisted for at least one week after the cessation of the stressor. In contrast, depressive-like behaviors were not elicited by SDR as assessed by the forced swim test or the tail suspension test. These data indicate that social disruption stress causes an increase in anxiety-like behaviors, but not depressivelike behaviors.

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Stable individual differences in physiological response to stressors: implications for stress-elicited changes in immune related health

Cited by 114 publications

References 27 publications

Neural sensitivity to social rejection is associated with inflammatory responses to social stress

Neural sensitivity to social rejection is associated with inflammatory responses to social stress

Leukocyte responsiveness, a quantitative assay for subjective mental workload

Repeated social defeat causes increased anxiety-like behavior and alters splenocyte function in C57BL/6 and CD-1 mice

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