protective and damaging effects of stress mediators (stress and the immune system) chapter four...
TRANSCRIPT
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Protective and Damaging Effects of Stress Mediators
(Stress and the Immune System)Chapter Four
Caitlin Cleary
June 13, 2007
http://www.kf6nvr.net/blog/archives/images/computing_stress.jpg
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Psychoneuroimmunology
• Scientific field investigating the link between bidirectional communications among the nervous system, endocrine and immune systems
– What are the implications of these linkages for physical and mental health?
- Stress!!!
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What is stress?
• A specific response by the body to a stimulus that disturbs or interferes with normal physiological equilibrium/homeostasis
• Stressors: can be real, imagined, internal or external– Physical/environmental– Natural disasters– Major life changes (good and bad)– Hassles/day-to-day aggravations– Personality related
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Stress - cross talk between CNS and immune system
• The brain is the master controller of the nervous, endocrine, and immune system
– However, the brain is also a target for these systems
– Subject to both protection and damage
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New Terms
• Allostasis: superordinate system by which stability is achieved through change – Primary mediators: HPA axis, catecholamines, and
cytokines– When set homeostatic points are out of boundaries, it
is referred to as allostatic states (ex. hypertension, cytokines increasing risk for autoimmune/inflammatory disorder)
• Allostatic load and allostatic overload: the cumulative wear and tear on the regulatory systems of the brain and body from the cumulative result of an allostatic state
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Peripheral Limbs of the Stress System: Part One
HPA axis: hypothalamic-pituitary-adrenal axis which regulates body processes including digestion, immune system, mood/sexuality, energy usage
Regulates hormone levels and maintains homeostasis
http://cti.itc.virginia.edu/~psyc220/kalat/JK367.fig12.6.HPA_axis.jpg
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Peripheral Limbs of the Stress System: Part Two, Autonomic Nervous System
• Involuntary activities that maintain homeostasis – i.e., cardiovascular, respiratory, and digestive functions, etc.
• Sympathetic and Parasympathetic branches that work complementary to each other
http://www.buteyko.co.nz/asthma/facts/images/nervous.jpg
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Normal Stress Response
Prey sees a predator
The event initiates stress response
The prey is able to escape predation
Stress response dissipates and body returns to homeostasis
“Fight or Flight” or “Tend and Befriend”
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Complicated Stress Interactions
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Stress induces change for adaptation
• Behavioral/Psychological (changes to eating, sleeping patterns, mood, etc.)
• Physiological (increased blood pressure, heart rate, dry throat, etc.)
• Immunological (suppression of immune system)
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“The General Adaptation Syndrome”
Hans Selye (1936)/ Cannon (1932) : the general adaptation syndrome, a classic, stereotyped theory of stress
1) Alarm reaction: adrenal medulla releases epinephrine, and the adrenal cortex produces glucocorticoids, promoting adaptation and restoring homeostasis (allostasis)
2) Resistance: defense and adaptation are optimal (allostatic load)
3) Exhaustion: persistence of stress response – which may lead to illness or death (allostatic overload)
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Chronic Stress Effects
• Consistently elevated cortisol and catecholamine levels (Stress response chronically activated)
• Non immune related: Diabetes, insomnia, myocardial infarction
• Stressful events predispose to disease and immune deregulation – infection, cancer, autoimmune diseases (ms)
• Impaired learning – atrophy in hippocampus• Depression (resulting from altered immune
function)
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Non-immune related allostatic overload
Glucocorticoids regulate behaviors that control energy input and expenditure - energy conversion serves the body well in the short term- elevated insulin levels (glucose uptake) and glucocorticoids promotes deposition of body fat and the formation of atherosclerotic plaques in the coronary arteries in the long term
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Immune related allostatic overload• These glucocorticoids can modulate the immune system
by lowering the Th1 response and increasing the Th2 response (diminishing cell mediated immune response)
• Cortisol, a specific glucocorticoid, and catecholamines can cause changes in proliferation, cytokine secretion, antibody production, cellular trafficking, and cytolytic processes
• It has been shown that adding CRH in vivo causes NK cell cytotoxicity to go down
• Clinical administration of glucocorticoids, such as cortisol, cause eosinophil and lymphocyte numbers to decrease
• Products of the Immune system also can react with the HPA axis. IL-1, a cytokine produced by the immune system to mediate inflammation, causes ACTH release indirectly by increasing CRH
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QUESTIONS?