Interelation between psyche neural system and, endocrin systems in regulationg the inmmune system response
psychoneuroendocrinoimmunology
Communication between the brain and immune system[edit]
Stimulation of brain sites alters immunity (stressed animals have altered immune systems).
Damage to brain hemispheres alters immunity (hemispheric lateralization effects).[39]
Immune cells produce cytokines that act on the CNS.
Immune cells respond to signals from the CNS.
Corticotropin-releasing hormone (CRH)[edit]
Release of corticotropin-releasing hormone (CRH) from the hypothalamus is influenced by stress.[44]CRH is a major regulator of the HPA axis/stress axis.
CRH Regulates secretion of adrenocorticotropic hormone (ACTH).
CRH is widely distributed in the brain and periphery
CRH also regulates the actions of the Autonomic nervous system ANS and immune system.
Furthermore, stressors that enhance the release of CRH suppress the function of the immune system; conversely, stressors that depress CRH release potentiate immunity.Central mediated since peripheral administration of CRH antagonist does not affect immunosuppression.
HPA axis/stress axis responds consistently to stressors that are new, unpredictable and that have low-perceived control.[44]
As cortisol reaches an appropriate level in response to the stressor, it deregulates the activity of the hippocampus, hypothalamus, and pituitary gland which results in less production of cortisol.[44]
Damage to brain hemispheres alters immunity (hemispheric lateralization effects).[39]
Immune cells produce cytokines that act on the CNS.
Immune cells respond to signals from the CNS.
Glucocorticoids and catecholamines influence immune cells.[40][41]
Hypothalamic Pituitary Adrenal axis releases the needed hormones to support the immune system.[42]
Activity of the immune system is correlated with neurochemical/neuroendocrine activity of brain cells.
Hypothalamic Pituitary Adrenal axis releases the needed hormones to support the immune system.[42]
Activity of the immune system is correlated with neurochemical/neuroendocrine activity of brain cells.
Anti-inflammatory hormones that enhance the organism's response to a stressor.
Prevent the overreaction of the body's own defense system.
Overactivation of glucocorticoid receptors can lead to health risks.[43]
Regulators of the immune system.
Affect cell growth, proliferation and differentiation.
Prevent the overreaction of the body's own defense system.
Overactivation of glucocorticoid receptors can lead to health risks.[43]
Regulators of the immune system.
Affect cell growth, proliferation and differentiation.
Cause immunosuppression which can lead to an extended amount of time fighting off infections.[43]
High basal levels of cortisol are associated with a higher risk of infection.[43]
Suppress cell adhesion, antigen presentation, chemotaxis and cytotoxicity.
Increase apoptosis.
High basal levels of cortisol are associated with a higher risk of infection.[43]
Suppress cell adhesion, antigen presentation, chemotaxis and cytotoxicity.
Increase apoptosis.
Corticotropin-releasing hormone (CRH)[edit]
Release of corticotropin-releasing hormone (CRH) from the hypothalamus is influenced by stress.[44]CRH is a major regulator of the HPA axis/stress axis.
CRH Regulates secretion of adrenocorticotropic hormone (ACTH).
CRH is widely distributed in the brain and periphery
CRH also regulates the actions of the Autonomic nervous system ANS and immune system.
Furthermore, stressors that enhance the release of CRH suppress the function of the immune system; conversely, stressors that depress CRH release potentiate immunity.Central mediated since peripheral administration of CRH antagonist does not affect immunosuppression.
HPA axis/stress axis responds consistently to stressors that are new, unpredictable and that have low-perceived control.[44]
As cortisol reaches an appropriate level in response to the stressor, it deregulates the activity of the hippocampus, hypothalamus, and pituitary gland which results in less production of cortisol.[44]
Psychological stress is regulated by the prefrontal cortex (PFC)
The PFC modulates vagal activity[45]
Prefrontally modulated and vagally mediated cholinergic input to the spleen reduces inflammatory responses[46]
The PFC modulates vagal activity[45]
Prefrontally modulated and vagally mediated cholinergic input to the spleen reduces inflammatory responses[46]
Source Wikipedia.
https://en.wikipedia.org/wiki/Psychoneuroimmunology
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