Khalid Z Matalka1. 1. Faculty of Pharmacy and Medical Technology, University of Petra, Amman, Jordan. kzm@uop.edu
Abstract
OBJECTIVES: Previously, a large number of studies reported that psychological stress and psychiatric illness reduces immune responsiveness. However, it turned out that stress reduces immune responsiveness is an oversimplified statement because the interactions between central nervous system, endocrine system and the immune system are undoubtedly complex. Therefore, this study aims in reviewing mental stress models (e.g. brief and written examination stress as subacute and acute type of stressor) that have been utilized to understand the effect of stress on the neuroendocrine and immune systems. METHODS: The published findings from human mental stress models on catecholamines, cortisol, prolactin levels and on T helper (Th) 1 and 2-induced cytokines are presented and discussed with respect to the in vitro and in vivo effects of glucocorticoids, catecholamines, and prolactin on the induction of cytokines. RESULTS: This review shows evidence that short-time (minutes) or preparation to a written examination, in those students who are stressed, induces the production of proinflammatory cytokines which may be related to Th1 response. However, longer mental stress (days) causes dysregulation in the immune function by shifting the cytokine response to Th2 response. CONCLUSIONS: The outcome from neuroendocrine and immune function prior to, following and after mental stress depends on multiple variables most importantly on the amount of stress, exposure time, coping behavior and adjustment of the individual. A few minutes of stress may improve immune performance but longer times of mental stress have detrimental effects that may lead to loss of immune integrity. Furthermore, studies on stress and common heath problems are necessary to increase our knowledge and understanding of the mechanisms responsible for producing neuroendocrine-induced immune changes in health and common diseases.
OBJECTIVES: Previously, a large number of studies reported that psychological stress and psychiatric illness reduces immune responsiveness. However, it turned out that stress reduces immune responsiveness is an oversimplified statement because the interactions between central nervous system, endocrine system and the immune system are undoubtedly complex. Therefore, this study aims in reviewing mental stress models (e.g. brief and written examination stress as subacute and acute type of stressor) that have been utilized to understand the effect of stress on the neuroendocrine and immune systems. METHODS: The published findings from human mental stress models on catecholamines, cortisol, prolactin levels and on T helper (Th) 1 and 2-induced cytokines are presented and discussed with respect to the in vitro and in vivo effects of glucocorticoids, catecholamines, and prolactin on the induction of cytokines. RESULTS: This review shows evidence that short-time (minutes) or preparation to a written examination, in those students who are stressed, induces the production of proinflammatory cytokines which may be related to Th1 response. However, longer mental stress (days) causes dysregulation in the immune function by shifting the cytokine response to Th2 response. CONCLUSIONS: The outcome from neuroendocrine and immune function prior to, following and after mental stress depends on multiple variables most importantly on the amount of stress, exposure time, coping behavior and adjustment of the individual. A few minutes of stress may improve immune performance but longer times of mental stress have detrimental effects that may lead to loss of immune integrity. Furthermore, studies on stress and common heath problems are necessary to increase our knowledge and understanding of the mechanisms responsible for producing neuroendocrine-induced immune changes in health and common diseases.
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