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Stress and depression-induced immune dysfunction: implications for the development and progression of cancer.
Int Rev Psychiatry 2005; 17(6):515-27IR

Abstract

The persistent activation of the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal-medullary axes in chronic stress response and in depression impairs the immune response and contributes to the development and progression of some types of cancer. This overview presents results from experimental animal models, human studies, and clinical evidence that various cellular and molecular immunological parameters are compromised in chronic stress and depression. At the cellular level, stressed and depressed patients had overall leukocytosis, high concentrations of circulating neutrophils, reduced mitogen-stimulated lymphocyte proliferation and neutrophil phagocytosis. At the molecular level, high levels of serum basal cortisol, acute phase proteins, specific antibodies against herpes simplex virus type 1 and Epstein Barr virus, plasma concentration of interleukins IL-1, IL-6, and TNF-alpha, and a shift in the balance of Th1 and Th2 immune response were observed. Both stress and depression were associated with the decreased cytotoxic T-cell and natural killer cell activities affecting the processes of the immune surveillance of tumours, and the events that modulate the development and the accumulation of somatic mutations and genomic instability. DNA damage, growth and angiogenic factors, proteases, matrix metalloproteinases, and reactive oxygen species were also related to the chronic stress response and depression. Behavioural strategies, psychological, and psychopharmacotherapeutic interventions that enhance effective coping and reduce affective distress showed beneficial effects in cancer patients. A better understanding of the bidirectional communication between the neuroendocrine and immune systems could contribute to novel clinical and treatment strategies in oncology.

Authors+Show Affiliations

Department of Pathology, Clinical Analysis and Toxicology, State University of Londrina, Londrina, Paraná, Brazil. reiche@sercomtel.com.brNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16401550

Citation

Reiche, Edna Maria Vissoci, et al. "Stress and Depression-induced Immune Dysfunction: Implications for the Development and Progression of Cancer." International Review of Psychiatry (Abingdon, England), vol. 17, no. 6, 2005, pp. 515-27.
Reiche EM, Morimoto HK, Nunes SM. Stress and depression-induced immune dysfunction: implications for the development and progression of cancer. Int Rev Psychiatry. 2005;17(6):515-27.
Reiche, E. M., Morimoto, H. K., & Nunes, S. M. (2005). Stress and depression-induced immune dysfunction: implications for the development and progression of cancer. International Review of Psychiatry (Abingdon, England), 17(6), pp. 515-27.
Reiche EM, Morimoto HK, Nunes SM. Stress and Depression-induced Immune Dysfunction: Implications for the Development and Progression of Cancer. Int Rev Psychiatry. 2005;17(6):515-27. PubMed PMID: 16401550.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Stress and depression-induced immune dysfunction: implications for the development and progression of cancer. AU - Reiche,Edna Maria Vissoci, AU - Morimoto,Helena Kaminami, AU - Nunes,Sandra Morimoto Vargas, PY - 2006/1/13/pubmed PY - 2006/4/4/medline PY - 2006/1/13/entrez SP - 515 EP - 27 JF - International review of psychiatry (Abingdon, England) JO - Int Rev Psychiatry VL - 17 IS - 6 N2 - The persistent activation of the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal-medullary axes in chronic stress response and in depression impairs the immune response and contributes to the development and progression of some types of cancer. This overview presents results from experimental animal models, human studies, and clinical evidence that various cellular and molecular immunological parameters are compromised in chronic stress and depression. At the cellular level, stressed and depressed patients had overall leukocytosis, high concentrations of circulating neutrophils, reduced mitogen-stimulated lymphocyte proliferation and neutrophil phagocytosis. At the molecular level, high levels of serum basal cortisol, acute phase proteins, specific antibodies against herpes simplex virus type 1 and Epstein Barr virus, plasma concentration of interleukins IL-1, IL-6, and TNF-alpha, and a shift in the balance of Th1 and Th2 immune response were observed. Both stress and depression were associated with the decreased cytotoxic T-cell and natural killer cell activities affecting the processes of the immune surveillance of tumours, and the events that modulate the development and the accumulation of somatic mutations and genomic instability. DNA damage, growth and angiogenic factors, proteases, matrix metalloproteinases, and reactive oxygen species were also related to the chronic stress response and depression. Behavioural strategies, psychological, and psychopharmacotherapeutic interventions that enhance effective coping and reduce affective distress showed beneficial effects in cancer patients. A better understanding of the bidirectional communication between the neuroendocrine and immune systems could contribute to novel clinical and treatment strategies in oncology. SN - 0954-0261 UR - https://www.unboundmedicine.com/medline/citation/16401550/Stress_and_depression_induced_immune_dysfunction:_implications_for_the_development_and_progression_of_cancer_ L2 - http://www.tandfonline.com/doi/full/10.1080/02646830500382102 DB - PRIME DP - Unbound Medicine ER -