Odborné studie a literatura

The effect of academic stress on immune function, as measured by the rate of secretion of salivary secretory immunoglobulin A (s-IgA), was studied prospectively in 64 first-year dental school students. Perceived stress and s-IgA secretion rate were measured five times–during an initial low-stress period, three high-stress periods coinciding with major examinations, and a final low-stress period. The s-IgA secretion rate was significantly lower in high-stress than low-stress periods for the whole group. In addition, personality characteristics differentiated patterns of s-IgA secretion rates. Students characterised by a great need to establish and maintain warm personal relationships secreted more s-IgA at each point than did all other subjects. The s-IgA secretion rates of those with a high inhibited need for power continued to decline through the final low-stress period rather than recovering as in all other subjects.

Zdroj studie: http://www.ncbi.nlm.nih.gov/pubmed/6134179

The purpose of this study was to examine the direct and stress-buffering effect of optimism and satisfaction with social support on immune responses in women with breast cancer. Participants were 54 post-operative (M = 19 days) breast cancer patients who completed questionnaires on stress, optimism, and satisfaction with social support and provided blood to measure natural killer cell activity (NKCA) and interferon-gamma (IFN-gamma) from whole blood. Higher levels of stress were associated with decrements in NKCA and IFN-gamma. Optimism moderated the relationship of stress on NKCA but was not related to IFN-gamma. Satisfaction with social support was unrelated to immune responses. Results suggest that interventions aimed at reducing stress and enhancing optimism in women with breast cancer might promote optimal immune response

Zdroj studie: http://www.ncbi.nlm.nih.gov/pubmed/17243109

OBJECTIVE: This study evaluated relations among optimism, depression, anger suppression and natural killer cell cytotoxicity (NKCC) in 61 men treated for localized prostate cancer (PC). METHOD: All participants were assessed at a single time point where demographics, optimism, depression and anger suppression were measured. We also collected peripheral venous blood to assess NKCC. RESULTS: Results showed that greater optimism was associated with greater NKCC (beta=.27, P<.05), less depression (beta=-.63, P<.001) and less anger suppression (beta=-.29, P<.05). Furthermore, less anger suppression (beta=-.35, P<.01) was associated with greater NKCC. In a hierarchical regression model controlling for depression and then anger suppression, the relationship between optimism and NKCC became nonsignificant [beta=.18, t(56)=1.51, P=.14], while anger suppression remained significantly correlated with NKCC [beta=-.29, t(56)=-2.40, P<.05]. CONCLUSIONS: Results suggest that optimism is associated with NKCC and a greater ability to adaptively express anger. Furthermore, it appears that less anger suppression partially mediates the relationship between optimism and NKCC.

Zdroj studie: http://www.ncbi.nlm.nih.gov/pubmed/16581368

This article introduces the supplement Advances in Cancer and Brain, Behavior, and Immunity and outlines important discoveries, paradigm shifts, and methodological innovations that have emerged in the past decade to advance mechanistic and translational understanding of biobehavioral influences on tumor biology, cancer treatment-related sequelae, and cancer outcomes. We offer a heuristic framework for research on biobehavioral pathways in cancer. The shifting survivorship landscape is highlighted, and we propose that the changing demographics suggest prudent adoption of a life course perspective of cancer and cancer survivorship. We note opportunities for psychoneuroimmunology (PNI) research to ameliorate the long-term, unintended consequences of aggressive curative intent and call attention to the critical role of reciprocal translational pathways between animal and human studies. Lastly, we briefly summarize the articles included in this compilation and offer our perspectives on future research directions.

Zdroj studie: http://www.sciencedirect.com/science/article/pii/S0889159113000068

The influence of psychosocial factors on the development and progression of cancer has been a longstanding hypothesis since ancient times. In fact, epidemiological and clinical studies over the past 30 years have provided strong evidence for links between chronic stress, depression and social isolation and cancer progression. By contrast, there is only limited evidence for the role of these behavioral factors in cancer initiation. Recent cellular and molecular studies have identified specific signaling pathways that impact cancer growth and metastasis. This article provides an overview of the relationship between psychosocial factors, specifically chronic stress, and cancer progression.

Zdroj studie: http://www.futuremedicine.com/doi/abs/10.2217/fon.10.142

The links between the psychological and physiological features of cancer risk and progression have been studied through psychoneuroimmunology. The persistent activation of the hypothalamic-pituitary-adrenal (HPA) axis in the chronic stress response and in depression probably impairs the immune response and contributes to the development and progression of some types of cancer. Here, we overview the evidence that various cellular and molecular immunological factors are compromised in chronic stress and depression and discuss the clinical implications of these factors in the initiation and progression of cancer. The consecutive stages of the multistep immune reactions are either inhibited or enhanced as a result of previous or parallel stress experiences, depending on the type and intensity of the stressor and on the animal species, strain, sex, or age. In general, both stressors and depression are associated with the decreased cytotoxic T-cell and natural-killer-cell activities that affect processes such as immune surveillance of tumours, and with the events that modulate development and accumulation of somatic mutations and genomic instability. A better understanding of the bidirectional communication between the neuroendocrine and immune systems could contribute to new clinical and treatment strategies.

Zdroj studie: http://www.sciencedirect.com/science/article/pii/S1470204504015979

It is becoming increasingly clear that stressful life events can affect cancer growth and metastasis by modulating nervous, endocrine, and immune systems. The purpose of this review is to briefly describe the process by which stress may potentiate carcinogenesis and how reducing body stress may prevent cancer growth and progression. The opioid peptide β-endorphin plays a critical role in bringing the stress axis to a state of homeostasis. We have recently shown that enhancement of endogenous levels of β-endorphin in the hypothalamus via β-endorphin neuron transplantation suppresses stress response, promotes immune function, and reduces the incidence of cancer in rat models of prostate and breast cancers. The cancer-preventive effect of β-endorphin is mediated through the suppression of sympathetic neuronal function, which results in increased peripheral natural killer cell and macrophage activities, elevated levels of anti-inflammatory cytokines, and reduced levels of inflammatory cytokines. β-endorphin inhibition of tumor progression also involves alteration in the tumor microenvironment, possibly because of suppression of catecholamine and inflammatory cytokine production, which are known to alter DNA repair, cell-matrix attachments, angiogenic process, and epithelial–mesenchymal transition. Thus, β-endorphin cell therapy may offer some therapeutic value in cancer prevention. Cancer Res; 72(4); 836–40. ©2012 AACR.

Zdroj studie: http://cancerres.aacrjournals.org/content/72/4/836.short

It long has been suspected that psychosocial factors affect cancer development and progression. Although the connections between stress and cancer causation are not strong, epidemiologic and clinical studies have provided strong links between cancer progression and several stress-related factors including chronic stress, depression, and social isolation. Recent molecular and biological studies have identified specific signaling pathways that influence cancer growth and metastasis. In particular, stress hormones can have a significant impact on protecting cancer cells from undergoing the anoikis form of programmed cell death, thus, providing a mechanistic advantage for metastasis. This review provides an overview of the relationship between psychosocial factors and the avoidance of anoikis by cancer cells. Cancer Prev Res; 4(4); 481–5. ©2011 AACR.

Zdroj studie: http://cancerpreventionresearch.aacrjournals.org/content/4/4/481.short

Clinical and animal studies now support the notion that psychological factors such as stress, chronic depression, and lack of social support might promote tumor growth and progression. Recently, cellular and molecular studies have started to identify biological processes that could mediate such effects. This review provides a mechanistic understanding of the relationship between biological and behavioral influences in cancer and points to more comprehensive behavioral and pharmacological approaches for better patient outcomes.

Zdroj studie: http://www.sciencedirect.com/science/article/pii/S0889159108002961

Depression has been characterized as a disorder of both immune suppression and immune activation. Markers of impaired cellular immunity (decreased natural killer cell cytotoxicity) and inflammation (elevated IL-6, TNFα, and CRP) have been associated with depression. These immunological markers have been associated with other medical illnesses, suggesting that immune dysregulation may be a central feature common to both depression and to its frequent medical comorbidities. Yet the significant associations of findings of both immune suppression and immune activation with depression raise questions concerning the relationship between these two classes of immunological observations. Depressed populations are heterogeneous groups, and there may be differences in the immune profiles of populations that are more narrowly defined in terms of symptom profile and/or demographic features.

There have been few reports concurrently investigating markers of immune suppression and immune activation in the same depressed individuals. An emerging pre-clinical literature suggests that chronic inflammation may directly contribute to the pathophysiology of immune suppression in the context of illnesses such as cancer and rheumatoid arthritis. This literature provides us with specific immunoregulatory mechanisms mediating these relationships that could also explain differences in immune disturbances between subsets of depressed individuals We propose a research agenda emphasizing the assessment of these immunoregulatory mechanisms in large samples of depressed subjects as a means to define the relationships among immune findings (suppression and/or activation) within the same depressed individuals and to characterize subsets of depressed subjects based on shared immune profiles. Such a program of research, building on and integrating our knowledge of the psychoneuroimmunology of depression, could lead to innovation in the assessment and treatment of depression and its medical comorbidities.

Zdroj studie: http://www.sciencedirect.com/science/article/pii/S0889159110005143

Conclusive evidence demonstrates that stressful events are related to immune change. For acute stressors, this relationship is causal, and it is reasonable to interpret causality from chronic stressors as well. The present review explores an aspect of the stress response with significant theoretical and clinical implications: subjective experiences of stress. Perceptions of stress and emotional distress are proposed to be the mechanisms by which events elicit immune change. In addition, subjective stress has been used to explain between-subject variability in the immunological stress response, and clinical researchers seek to mitigate the immunological consequences of stress by improving subjective stress. These interpretations persist despite modest support for an association between subjective stress and immune function.

Two potential solutions to this dilemma are explored. First, longitudinal data may better illuminate the role of subjective stress in immune function than do cross-sectional studies. A few data suggest that change in subjective stress is more relevant for immune function than are absolute levels [89, 140, 141], but more research is needed to establish this. Second, it is possible that the appraisal of events as stressful is not always accessible to the conscious mind [14]. Participants using repression or denial may not be aware of feelings of stress, yet may show stress-related physiological reactions. Consistent evaluation of such traits is needed to evaluate this possibility.

Clarification of the role of subjective stress in immune change has both theoretical and clinical implications. It will further our understanding of how stressful events modulate immune activity as well as identifying targets for psychological intervention. With these tools in hand, we become better equipped to improve the health and quality of life for those enduring chronic stress.

Zdroj studie: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2473865/