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Chapter 8

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Gordon Anderson

PSY333 CHAPTER 8 – IMMUNITY, STRESS, AND DISEASE - autonomic nervous system sends nerves into tissues that form or store the cells of the immune system, and eventually enter the circulation - tissues of the immune system are sensitive to the hormones that are released by the pituitary under the control of the brain (those that it has receptors for at least) conditioned immunosuppression – present an animal with a drug that suppress the immune system, and present a “conditioned stimulus” such as an artificially flavoured drink - present the drink by itself next time, and immune system function will go down Immune System Basics - immune system defends the body against infectious agents (ex. Viruses, bacteria, fungi, and parasites) - immune defences brought by lymphocytes/monocytes (known as white blood cells collectively) - two types of lymphocytes o T cells – originate in bone marrow, migrate to thymus  Several kinds of T cells (T helper, T suppressor cells, cytotoxic killers, etc.) o B cells - originate in bone marrow, mature in bone marrow  Produce antibodies - T/B cells attack infectious agents o T cells: cell-mediated immunity (page 141)  When infectious agent invades the body, recognized by a macrophage (type of monocyte), and presents the foreign particle to a T helper cell  T cells begin to proliferate in response to the invasion  Results in activation and proliferation of cytotoxic killer cells which attack and destroy the infectious agent  Ex. T-cell component of the immune system is knocked out by AIDS virus o B cells: anti-body mediated immunity (page 142)  Once macrophage T-helper cell collaboration occurred, T helper cells stimulate B-cell proliferation  Main task of B-cells: differentiate and generate antibodies, large proteins that will recognize and bind to some specific feature of the invading infectious agent  Antibody formed has unique shape – it conforms perfectly to shape of distinctive feature of invader (ex. Like the fit between lock and key)  In binding to specific feature, antibodies immobilize the infectious agent and target it for destruction - Cytokines – communicate between different cell types o When macrophages first recognize an infectious agent, interleukin-1 is released (messenger) o Triggers T helper cell to release interleukin-2 (stimulates T-cell growth) o On antibody front, T cells secrete B-cell growth factor o Other classes of messengers, (ex. Interferons – activate broad classes of lymphocytes) - What if something goes wrong with the immune system’s sorting? (between what belongs to you, and what doesn’t) o Immune system could miss infectious invader  Or decides something is dangerous invader that really isn’t o Immune system overreacts, and a normal part of your own body is mistaken for an infectious agent and is attacked  Autoimmune diseases may result • Ex. Multiple sclerosis/juvenile diabetes - Acquired immunity PSY333 CHAPTER 8 – IMMUNITY, STRESS, AND DISEASE o Acquire the ability to target pathogen X specifically, with antibodies and cell-mediated immunity that specifically recognize that pathogen o Takes time to build up that immunity when you are first exposed to pathogen X – involves finding which antibody has the best fit and generating a zillion copies of it o While you will now be geared up to specifically go after pathogen X for a long time to come once that specific defense is on line, repeated exposure to pathogen X will boost those targeted defenses even more - Acquired immunity found only in vertebrates - Innate immunity o Don’t bother acquiring the means to target pathogen X specifically with antibodies that will be different from those that would target, ex. Pathogen Y o The second any sort of pathogen hits your system, this NON-specific immune response swings into action  General response tends to occur at the beachhead where a pathogen gets its first foothold (ex. Skin or moist mucosal tissue (mouth/nose)) - Saliva contains class of antibodies that generically attack any sort of microbe that it encounters o Antibodies are secreted and coat mucosal surfaces o At the site of infection, capillaries loosen up, allowing cells of the innate immune response to slip out of circulation to infiltrate the immediate area of infection  Cells include macrophages, neutrophils, and natural killer cells • Which attack microbe o Loosening of capillaries allows fluid containing proteins that can fight the invasive microbes to flow in from circulation o Proteins fight the microbe, but fluid also makes area swell up – edema o Innate immune system is leaping into action causing inflammation How Does Stress Inhibit Immune Function? Stress: - suppress formation of new lymphocytes and their release into circulation, as well as shorten the time pre-existing lymphocytes stay in circulation - inhibit manufacturing of new antibodies in response to an infectious agent, disrupt communication among lymphocytes through the release of relevant messengers - inhibit innate immune response, suppressing inflammation Immune suppression occurs via glucocorticoids - glucocorticoids o can cause shrinking of thymus gland o halt formation of new lymphocytes in the thymus (most of the thymic tissue is made up of these new cells, ready to be secreted into the bloodstream) o make circulating lymphocytes less responsive to an infectious alarm (because glucocorticoids inhibit the release of messengers like interleukins and interferons) o cause lymphocytes to be yanked out of circulation and stuck back in storage in immune tissues o most effects of glucocorticoids are against T cells as oppose to B cells  cell-mediated immunity is more disrupted than anti-body mediated immunity o kill lymphocytes  “programmed cell death” • glucocorticoids can trigger suicide pathways into action in lymphocytes, through a variety of mechanisms PSY333 CHAPTER 8 – IMMUNITY, STRESS, AND DISEASE - sympathetic nervous system hormones (beta-endorphin/CRH) can also play a role in suppressing immunity during stress – effects not well documented Why is Immunity Suppressed During Stress? - stress causes active expenditure of energy in order to disassemble the pre-existing immune system – tissues are shrunk, cells are destroyed - during infections o immune system releases interleukin-1, which stimulates hypothalamus to release CRH o CRH stimulates pituitary to release ACTH, which causes adrenals to release glucocorticoids  This suppresses the immune system o THEREFORE, under some circumstances  Immune system will ask body to secrete hormones that will ultimately suppress the immune system • Don’t know the reason Surprise - during first few minutes of stress (up to about thirty) after onset of stressor – don’t uniformly suppress immunity – enhance many aspects of it o shown with all realms of immunity but particularly innate immunity  more immune cells rushed into circulation and, in the injured nervous system, more inflammatory cells infiltrate the site of injury  circulating lymphocytes better at releasing and responding to immune messengers  more generic antibodies of innate immune system are released into saliva - by one hour: more sustained glucocorticoid and sympathetic activation begins to suppress immunity o If stressors ends then, immune function goes back to where it started (baseline) - Only with major stressors of longer duration, or really major exposure to glucocorticoids that immune system does not just return to baseline, and plummets into a range that qualifies as immunosuppression o Sustained major stressors drive numbers down to 40-70% below baseline - Immune systems that are chronically activated: begin to mistake part of you for being something invasive  leading to autoimmune disease - Stress response makes sure that immune activation doesn’t spiral into autoimmunity - Some aspects that have been taken to be aspects of immune suppression are actually more subtle versions of immune enhancement: o Subtle rise in glucocorticoid levels for a short time (start of phase B) – hormones kill only particular set of lymphocytes – older ones, ones that don’t work as well  Glucocorticoids – helping to sculpt the immune response, getting rid of lymphocytes that aren’t ideal for immediate emergency  Glucocorticoids also yank some remaining lymphocytes out of circulation – transferring them to the front lines (specific site of infectious) so that the wounds heal faster Autoimmunity: 1. administration of large amounts of stress hormones makes autoimmune diseases less damaging (because by dramatically suppressing the immune system , it can no longer attack your nervous system, pancreas, etc.) makes autoimmune diseases less damaging PSY333 CHAPTER 8 – IMMUNITY, STRESS, AND DISEASE a. prolonged major stressors decrease the symptoms of autoimmune diseases in lab rats 2. stress can worsen autoimmune diseases a. subset of patients whose initial onset of an autoimmune disease, to an even greater extent, their intermittent flare-ups of bad symptoms are yoked to stress b. stress can worsen autoimmunity in animal models of these diseases: multiple sclerosis, rheumatoid arthritis, Grave’s disease, ulcerative colitis, inflammatory bowel disease, and asthma Increasing the risk of autoimmune disease: 1. numerous transient stressors (phases A and B) increase risk of autoimmunity 2. having phase A not followed by phase B increases risk of autoimmunity a. if you don’t have adequate phase B, pushes immune system spiral upward into autoimmunity - if you have hefty doses of glucocorticoids, or massive prolonged stress – put the system in phase C, results in dramatic immune suppression – decreases symptoms of autoimmunity - acute stress: rat models more at risk for multiple sclerosis, chronic stress suppresses symptoms of autoimmune disease and with numerous repetitions of coordinating various on- and-off switches which leads to something uncoordinated, that increases risk of system becoming autoimmune Testing the Stress-Disease Link Social Support and Social Isolation - fewer social relationships a person has, shorter their life expectancy is and the worse the impact of various infectious diseases - impact of social relationships on life expectancy appears to be at least as large as that of variables such as, cigarette smoking, hypertension, obesity, and level of physical activity - for the same illness, people with the fewest social connections have approximately 2.5 times as much chance of dying as those with the most connections - H
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