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Understanding the interaction between psychosocial stress and immune-related diseases: a stepwise progression.
Brain Behav Immun 2007; 21(8):1009-18BB

Abstract

For many years, anecdotal evidence and clinical observations have suggested that exposure to psychosocial stress can affect disease outcomes in immune-related disorders such as viral infections, chronic autoimmune diseases and tumors. Experimental evidence in humans supporting these observations was, however, lacking. Studies published in the last 2 decades in Brain, Behavior and Immunity and other journals have demonstrated that acute and chronic psychological stress can induce pronounced changes in innate and adaptive immune responses and that these changes are predominantly mediated via neuroendocrine mediators from the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal axis. In addition, psychological stress has predicted disease outcomes using sophisticated models such as viral challenge, response to vaccination, tracking of herpesvirus latency, exploration of tumor metastasis and healing of experimental wounds, as well as epidemiological investigations of disease progression and mortality. These studies have contributed significantly to our understanding that the neuroendocrine-immune interaction is disturbed in many pathophysiological conditions, that stress can contribute to this disturbance, and that malfunction in these communication pathways can play a significant role in the progression of disease processes. There are, however, significant gaps in the extant literature. In the coming decade(s), it will be essential to further analyze neuroendocrine-immune communication during disease states and to define the specific pathways linking the central nervous system to the molecular events that control important disease-relevant processes. This knowledge will provide the basis for new therapeutic pharmacological and non-pharmacological behavioral approaches to the treatment of chronic diseases via specific modulation of nervous system-immune system communication.

Authors+Show Affiliations

Health Psychology Program, Department of Psychiatry, University of California, San Francisco, CA 94143-0848, USA. kemenym@healthpsych.ucsf.eduNo affiliation info available

Pub Type(s)

Historical Article
Journal Article

Language

eng

PubMed ID

17889502

Citation

Kemeny, Margaret E., and Manfred Schedlowski. "Understanding the Interaction Between Psychosocial Stress and Immune-related Diseases: a Stepwise Progression." Brain, Behavior, and Immunity, vol. 21, no. 8, 2007, pp. 1009-18.
Kemeny ME, Schedlowski M. Understanding the interaction between psychosocial stress and immune-related diseases: a stepwise progression. Brain Behav Immun. 2007;21(8):1009-18.
Kemeny, M. E., & Schedlowski, M. (2007). Understanding the interaction between psychosocial stress and immune-related diseases: a stepwise progression. Brain, Behavior, and Immunity, 21(8), pp. 1009-18.
Kemeny ME, Schedlowski M. Understanding the Interaction Between Psychosocial Stress and Immune-related Diseases: a Stepwise Progression. Brain Behav Immun. 2007;21(8):1009-18. PubMed PMID: 17889502.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Understanding the interaction between psychosocial stress and immune-related diseases: a stepwise progression. AU - Kemeny,Margaret E, AU - Schedlowski,Manfred, Y1 - 2007/09/21/ PY - 2007/05/09/received PY - 2007/07/03/revised PY - 2007/07/04/accepted PY - 2007/9/25/pubmed PY - 2008/1/9/medline PY - 2007/9/25/entrez SP - 1009 EP - 18 JF - Brain, behavior, and immunity JO - Brain Behav. Immun. VL - 21 IS - 8 N2 - For many years, anecdotal evidence and clinical observations have suggested that exposure to psychosocial stress can affect disease outcomes in immune-related disorders such as viral infections, chronic autoimmune diseases and tumors. Experimental evidence in humans supporting these observations was, however, lacking. Studies published in the last 2 decades in Brain, Behavior and Immunity and other journals have demonstrated that acute and chronic psychological stress can induce pronounced changes in innate and adaptive immune responses and that these changes are predominantly mediated via neuroendocrine mediators from the hypothalamic-pituitary-adrenal axis and the sympathetic-adrenal axis. In addition, psychological stress has predicted disease outcomes using sophisticated models such as viral challenge, response to vaccination, tracking of herpesvirus latency, exploration of tumor metastasis and healing of experimental wounds, as well as epidemiological investigations of disease progression and mortality. These studies have contributed significantly to our understanding that the neuroendocrine-immune interaction is disturbed in many pathophysiological conditions, that stress can contribute to this disturbance, and that malfunction in these communication pathways can play a significant role in the progression of disease processes. There are, however, significant gaps in the extant literature. In the coming decade(s), it will be essential to further analyze neuroendocrine-immune communication during disease states and to define the specific pathways linking the central nervous system to the molecular events that control important disease-relevant processes. This knowledge will provide the basis for new therapeutic pharmacological and non-pharmacological behavioral approaches to the treatment of chronic diseases via specific modulation of nervous system-immune system communication. SN - 0889-1591 UR - https://www.unboundmedicine.com/medline/citation/17889502/Understanding_the_interaction_between_psychosocial_stress_and_immune_related_diseases:_a_stepwise_progression_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0889-1591(07)00160-2 DB - PRIME DP - Unbound Medicine ER -