No abstract available.
Depression* ; Immune System* ; Psychoneuroimmunology* ; Schizophrenia*

Psychosomatic medicine is a part of medicine which is to find the effect of psychological, behavioural, and medical factors on the human body and disease. In the early 20th century, the idea of psychogenesis had been developed and resulted in the concept of psychosomatic disease which was believed to be caused by psychological factors. However a multifactorial model of illness developed and it allowed illness to be viewed as a result of biopsychosocial interactions. The following have been highlighted by consultation-liaison psychiatry. Psychosomatic medicine has addressed stress and psychiatric factors which affect the etiology, course, and treatment of medical disorders. Moreover it contributes the growth of other related disciplines such as psychoneuroendocrinology, psychoimmunology, behavioral medicine, health psychology and quality of life research. Nowadays, psychosomatic field becomes enlarged because medical and surgical departments have been developed rapidly, and research methods and tools have brought forth rapid progress and advance in medical science. Therefore the author reviews the past and present psychosomatic researches and suggests the future of psychosomatic research in Korea.
Behavioral Medicine ; Human Body ; Korea ; Psychoneuroimmunology ; Psychosomatic Medicine ; Quality of Life

This review briefly summarizes the relevant knowledge of psychoneuroimmunological basis for neuroimmunology, with particular emphasis on bidirectional neural-immune interactions. The immune system and the nervous system maintain extensive communication, including hardwiring of sympathetic and parasympathetic nerves to lymphoid organs. Immune system is modulated by various neurotransmitters such as acetylcholine, norepinephrine, substance P and histamine. Neuroendocrine hormones such as corticotrophin-releasing hormone(CRH) or substance P regulate cytokine balance. The immune system modulates brain activity including sleep and body temperature. Recent studies have revealed that psychological factors which influence immunity and immune-related disease may modulate brain-to -immune interaction. But, we still await the scientific research and evidences to prove whether or how behavioral or treatment intervention of stress can influence the development, progress or prevention of a specific disease.
Acetylcholine ; Body Temperature ; Brain ; Histamine ; Immune System ; Nervous System ; Neurotransmitter Agents ; Norepinephrine ; Psychoneuroimmunology ; Substance P

PURPOSE: The purpose of this review was to describe a psychoneuroimmunology (PNI) framework for postpartum depression (PPD) and discuss its implications for nursing research and practice for postpartum women. METHODS: This study explored the role of hypothalamic-pituitary-adrenal (HPA) axis and inflammation as possible mediators of risk factors for PPD through literature review. RESULTS: From this PNI view, human bodies are designed to respond with the reciprocal interactions among the neuro-endocrine and immune system when they are faced with physical or psychological stressors. Chronic stress induces alterations in the function of HPA axis, and a chronic low-grade inflammatory response is associated with depression. The dysfunctions of cytokines and HPA axis have been observed during the postpartum period. Stress promotes glucocorticoid receptor resistance, which can promote inflammatory responses. This, in turn, can contribute to the pathophysiology of depression. This can especially affect populations at vulnerable time-points, such as women in the postpartum. CONCLUSION: From a PNI perspective, well-designed prospective research evaluating the role of stress and inflammation as an etiology of PPD and the effect of stress reduction is warranted to prevent PPD.
Axis, Cervical Vertebra ; Cytokines ; Depression ; Depression, Postpartum* ; Female ; Human Body ; Humans ; Immune System ; Inflammation ; Nursing Research ; Postpartum Period ; Psychoneuroimmunology ; Receptors, Glucocorticoid ; Risk Factors

Inflammation is an immune response engaged with the reciprocal interactions among the neural, endocrine and immune system. From this psychoneuroimmunological view, inflammation is one of important allostatic loads contributory to depression. Sickness behaviors in the inflammatory state share many parts of depressive symptoms and patients treated with cytokines for various illnesses are at increased risk of developing depression. The dysfunctions of cytokines and hypothalamic-pituitary-adrenal axis have been widely investigated to find out inflammatory responses. Inflammatory mediators such as cytokines, glucocorticoid and C-reactive protein affect the etiopathogenesis of depression via altered monoamine and glutamate neurotransmission, glucocorticoid receptor resistance and neurogenesis. Although inflammation is subtle and not easy to be detected in the wide population, it is basal pathophysiology and plays an important role at least to the vulnerable patients. From this perspectives, inflammatory markers may be useful in the diagnosis and prediction of treatment response, leading to the possibility of tailored treatments. Understanding depression as a kind of inflammatory disease would provide new opportunities for the psychiatry beyond monoamine theory.
Allostasis ; Axis, Cervical Vertebra ; C-Reactive Protein ; Cytokines ; Depression ; Glutamic Acid ; Humans ; Illness Behavior ; Immune System ; Inflammation ; Neurogenesis ; Psychoneuroimmunology ; Receptors, Glucocorticoid ; Synaptic Transmission

Stress can induce modifications in the central nervous(CNS), autonomic nervous and neuroendocrine system. Thus, the stress response has long been measured in laboratory experiments by biochemical changes in the hormone systems that are referred to as the sympathetic nervous system(SNS) and pituitary-adrenocortical axes(HPA). These axes react to acute stress or chronic stress. The activation of these two particular pathways result in elevated serum levels of catecholamines, cortisol, ACTH, dopamine, and others hormones. But there is considerable debate about the relevance of traditional laboratory stress findings to real-life situation. The neurobiology of stress is a key step to the understanding of stress-induced changes of immune functions. The immune system operates in communication with brain and endocrine system. Because of this extensive communication, the immune system can influence how we feel and behave. The stress are associated with endocrine and autonomic changes that can inhibit immune system function. The concept of neurocardiology renders plausible the various theoretical constructs of stress as they relate to circulatory vascular disease. Detailed reviews of the anatomic connections between the brain and the heart and of experimental and clinical data on the role of the CNS in cardiac dysfunction can be found elsewhere. In this study, we reviewed that stress was associated with cardiovascular disease mortality through the known cardiovascular risk factors(hypertension, heart rate variability, homocycteine, and clotting system).
Adrenocorticotropic Hormone ; Biomarkers* ; Brain ; Cardiovascular Diseases ; Catecholamines ; Dopamine ; Endocrine System ; Heart ; Heart Rate ; Hydrocortisone ; Immune System ; Mortality ; Neurobiology ; Neurosecretory Systems ; Psychoneuroimmunology ; Vascular Diseases

Accumulating evidence has suggested the existence of reciprocal communication between immune, endocrine, and neurotransmitter system. Cytokine hypothesis of depression implies that increased pro-inflammatory cytokine such as -1, IL-6, IL-12, TNF-alpha, and IFN-gamma in major depression, acting neuromodulators, play a key role in the mediation of behavioral, neuroendocrine, and neurochemical disturbances in depression. Concerning the relation between cytokines and serotonin metabolism, pro-inflammatory cytokines have profound effects on the metabolism of brain serotonin through the enzyme indoleamine-2,3-dioxygenase(IDO) that metabolizes tryptophan, the precursor of 5-HT to neurodegenerative quinolinate and neuroprotective kynurenate. The neurodegeneration process is reinforced by the neurotoxic effect of the hypercortisolemia during depression. From this perspective, it is possible that efficacy of antidepressants in the treatment of depression may, at least in part, rely on downregulation of pro-inflammatory cytokine synthesis. So, the use of cytokine synthesis inhibitors or cytokine antagonists may be a new treatment approach in depression. However, at present the question whether cytokines play a causal role in the onset of depression or are mere epiphenomena sustaining depressive symptoms remains to be elucidated. Nevertheless, cytokine hypothesis has created new perspectives in the study of psychological and pathophysiological mechanism that are associated with major depression, as well as the prospect for developing a new generation antidepressants.
Antidepressive Agents ; Brain ; Cytokines ; Depression ; Down-Regulation ; Interleukin-12 ; Interleukin-6 ; Kynurenic Acid ; Negotiating ; Neurotransmitter Agents ; Psychoneuroimmunology ; Quinolinic Acid ; Serotonin ; Tryptophan ; Tumor Necrosis Factor-alpha