this lecture was about psychoneuroimmunology, the study of how the mindset can influence and be influenced by the interplay between the nervous and immune systems. contrast this with neuroimmunomodulation, which is the study of how the central nervous system can produce changes in the immune system. we looked mainly at the interplay between stress (actually defined as the perception of the inadequacy to cope to a situation that compromises one's physiological or psychological well being), the neuropeptides that it produces in the CNS, and the ultimate effect that it has on the immune system.
the HPA axis, hypothalamus / pituitary / adrenal cortex releases cortisol in response to stress: stress causes the hypothalmus to release cortitropin releaseing hormone and arginine vasopressin, which triggers the pituitary to make adrenocorticotropic hormone, which triggers the adrenal cortex to make cortisol. in addition, glucocorticoids are secreted by the adrenal cortex. both of these substances produce a wide variety of effects within the immune system, including mediation of cytokine production, chemokine production, adhesion molecules, cell trafficking, proliferation. in particular, glucocorticoids can bind to "transcription receptors" on cytokine producing cells, which are then endocytosed and bind to "response elements" which up or downregulate the transcription of cytokines.
the SAM axis is the sympathetic adrenal medullary axis, and produces norepinephrine and epinephrine (catecholamines) alongside the HPA's production of cortisol and glucocorticoids in response to stress. adrenergic receptors for catecholamines are present on macrophages in two forms; alpha adrenergic receptors have a high affinity for catecholamines and therefore are active during low stress levels. beta adrenergic receptors have a low affinity, and therefore are active during high stress levels. the alpha adrenergic receptors act to stimulate the immune response by increasing phagocytosis, TNF-alpha production, IL-6 production. in contrast, binding to the beta adrenergic receptors decreases phagocytosis, decreases antigen processing and presentation, and decreases IL-12 production.
questions
neuroimmunomodulation...
1. what is the difference between psychoneuroimmunology and neuroimmunomodulation?
2. what was a "historical" example of neuroimmunomodulation?
3. what is an example of evidence of how the immune system affects the brain?
4. what is an example of how the central nervous system affects the immune system?
stress and the HPA axis...
5. describe how stress can trigger events in the HPA axis.
6. what is adrenal fatigue?
7. what are glucocorticoids and what are their role in the immune system?
8. how do glucocorticoids affect cytokine levels?
9. what is the theory for how cortisol affects the immune system?
SAM axis and opiods...
10. what is the SAM axis and what is its role in the immune system?
11. what is the effect of catecholamines on the immune system?
12. what are the two types of adrenergic receptors on macrophage and how do they relate to stress levels?
13. what are the effects of binding to the alpha adrenergic receptor?
14. what are the effects of binding to the beta adrenergic receptor?
15. how do opioids affect the immune system?
answers
1. neuroimmunomodulation is based on the premise that the nervous system can affect the immune system and vice versa. psychoneuroimmunology is the study of how the nervous and immune system interact with mood as well.
2. injecting LPS into someone can cause a fever- this implies that the immune response activates the HPA axis to secrete cortisol. we now know that the mechanism is related to macrophage's secretion of IL-1 that crosses the blood brain barrier.
3. the presence of IL-1 receptors in the brain; IL-1 makes you sleepy.
4. the innervation of lymph nodes, receptors on lymph nodes for certain neurotransmitters.
5. stress causes hypothalamus to release corticotropin releasing hormone and arginine vasopressin, which triggers the pituitary to make adrenocoricotropic hormone, which triggers adrenal cortex to make cortisol.
6. adrenal fatigue is the idea that chronic stress can eventually deplete cortisol levels, after an initial increase. the idea also states that cortisol and DHEA are similar hormones made from the same precursor, and that as cortisol levels increase, DHEA decreases; but that DHEA levels are maintained while cortisol levels eventually fall.
7. a hormone produced by the adrenal cortex that has diverse effects in the immune system, including mediation of cytokines, chemokines, adhesion molecules, cell trafficking, proliferation.
8. glucocorticoids bind to transcription receptors which are endocytosed upon binding and attach to "response elements" in front of cytokine genes, allowing it to upregulate or downregulate transcription of cytokine genes.
9. cortisol might play a role in preventing the immune system from being overstimulated. this has been evidenced in some rheumatoid arthritis patients who had increased disease activity when cortisol levels were blocked.
10. the sympathetic adrenal medullary axis; works in concert with the HPA axis by producing catecholamines.
11. similar to glucocorticoids produced by the HPA axis; cell proliferation, cytokine production, antibody production, cell trafficking. in general, catecholamines mediate the "fight or flight" response.
12. alpha adrenergic has a high affinity for catecholamines and therefore is active during low stress levels; beta adrenergic has a low affinity for catecholamines and therefore is active during high stress levels.
13. increases phagocytosis, increases TNF-alpha, increases IL-6.
14. decreases phagocytosis, decreases antigen processing and presentation, decreases production of IL-12.
15. decreases IL-12 production by macrophages, favoring a Th2 response.
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