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Schema of hypothalamus–pituitary–adrenal (HPA) axis of stress response.Abbreviations: ACTH, adrenocorticotropic hormone; CNS, central nervous system; CRH/AVP, corticotrophin-releasing hormone/arginine vasopressin; GCR, glucocorticoid receptor; IL, interleukin; TNF, tumor necrosis factor.
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f2-ijgm-2-019: Schema of hypothalamus–pituitary–adrenal (HPA) axis of stress response.Abbreviations: ACTH, adrenocorticotropic hormone; CNS, central nervous system; CRH/AVP, corticotrophin-releasing hormone/arginine vasopressin; GCR, glucocorticoid receptor; IL, interleukin; TNF, tumor necrosis factor.

Mentions: There are two parts to the stress response: sympathetic–adrenal–medullary (SAM) and the hypothalamic–pituitary–adrenal axis (HPA). The HPA is the core stress axis in mammals and together with the SAM system co-ordinates response to the diverse range of stressors from psychological to physical. There is considerable interplay between both neuronal systems especially between the noradrenergic nucleus locus ceruleus which provides central regulation of the SAM and the parvocellular neurones which regulate the HPA. The SAM, by triggering catecholamine release, provides the acute stress response whilst the HPA governs longer term stress defence mechanisms. Together those systems regulate energy utilisation and metabolic activity throughout the body.34 The SAM system produces the immediate shock response by acting on the hypothalamus, which activates the adrenal medulla and the sympathetic autonomic nervous system (ANS) (Figure 1). The SAM produces the “fight-or-flight” response which increases alertness, blood flow to muscles, heart rate, blood pressure, respiration rate, etc. and might decrease activity in the digestive system. The HPA system regulates release of the hormone CRF to activate the anterior pituitary and uses another hormone, adrenocorticotropic hormone (ACTH), to activate the adrenal cortex to release a group of hormones including cortisol (Figure 2). Cortisol and other glucocorticoid hormones have various effects such as conservation of glucose for neural tissues, elevation or stabilization of blood glucose levels, mobilization of protein reserves, conservation of salts and water, suppression of wound healing and the immune system. According to Seyle’s general adaptation syndrome (GAS) theory the general adaptation syndrome divides the stress response into three stages: Stage 1: Alarm reaction (SAM and HPA activity increases and result in the “fight-or-flight” response); Stage 2: Resistance (HPA activity takes over, bodily resources are at maximum and if the stress is experienced for short term the body returns to normalcy); Stage 3: Exhaustion (with very prolonged stress, bodily systems are ineffective. Sympathetic ANS action reappears. Adrenal cortex damage causes parasympathetic action, eg, energy storage failure. The immune system collapses, and stress-related diseases increase).

Modern approaches to understanding stress and disease susceptibility: A review with special emphasis on respiratory disease

Aich P, Potter AA, Griebel PJ - Int J Gen Med (2009)

Bottom Line: Little is known how stress affects disease susceptibility, yet understanding this mechanism is important for developing effective treatments, and for improving health and food quality.The current review focuses on (a) the effects of psychological stressors in humans and animals, (b) various methodologies employed to understand stress responses and their outcomes, and (c) the current status of the attempts to correlate stress and disease with respiratory disease as model system.These new approaches will also aid in our understanding how these processes are related to the dynamics and kinetics of changes in expression of multiple genes at various levels.

Affiliation: Vaccine and Infectious Disease Organization, University of Saskatchewan, Saskatoon, Canada.

ABSTRACT
Studies in animals and humans link both physical and psychological stress with an increased incidence and severity of respiratory infections. For this manuscript we define stress as the physiological responses an individual undergoes while adjusting to a continually changing environment. It is known that stressors of various types (psychological/physical) can alter the physiological levels of certain hormones, chemokines and cytokines. These alterations send information to the central nervous system to take necessary action which then sends messages to appropriate organs/tissues/cells to respond. These messages can either activate or suppress the immune system as needed and failure to compensate for this by the body can lead to serious health-related problems. Little is known how stress affects disease susceptibility, yet understanding this mechanism is important for developing effective treatments, and for improving health and food quality. The current review focuses on (a) the effects of psychological stressors in humans and animals, (b) various methodologies employed to understand stress responses and their outcomes, and (c) the current status of the attempts to correlate stress and disease with respiratory disease as model system. The methodologies included in this review span traditional epidemiological, behavioral and immunological studies to current high throughput genomic, proteomic, metabolomic/metabonomic approaches. With the advent of various newer omics and bioinformatics methodologies we postulate that it will become feasible to understand the mechanisms through which stress can influence disease onset. Although the literature in this area is limited because of the infancy of this research area, the objective of this review is to illustrate the power of new approaches to address complex biological questions. These new approaches will also aid in our understanding how these processes are related to the dynamics and kinetics of changes in expression of multiple genes at various levels.

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