HSM330 article 5 summary

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Department
Health Services Management
Course
HSM 330
Professor
Daolun Chen
Semester
Fall

Description
Eskandari - Neural-Immune Interactions in Health and Disease -immune system and CNS communicate -CNS signals immune system via hormonal & neuronal pathways and immune sysem sig nals CNS through similar routes via immune mediators & cytokines -primary hormonal pathway by which CNS regulates immune system is hypothalamic-p ituitary-adrenal (HPA) axis, through hormones of neuroendocrine stress response -sympathetic NS regulates immune system function primarily via adrenergic NTs re leased through neural routes -neuroendocrine regulaltion of immune function is essential for survival during stress/infection and to modulate immune responses in inflammatory disease -glucocorticoids are main effector endpoint of neuroendocrine response system -numerous routes by which immune, endocrine, and CNS communicate -CNS regulates immune system locally at sites of inflammation, regionally in imm une organs, and systemically through hormonal routes -immune system regulates CNS -ex: cytokines produced at an inflammatory site sig nal brain to produce symptoms of sickness-related behaviour and fever -interruptions/perturbations of these connective pathways can alter severity, co urse, and susceptibility and resistance to diseases CNS -several brain centers involved in immune regulation -2 major mechs through which CNS regulates immune system 1) the hormonal stress response through production of glucocorticoids 2) the autonomic NS w/ release of NE -hormonal stress response is mainly regulated via HPA axis -corticotropin-releasing hormone (CRH) is secreted from paraventricular nucleus of hypothalamus into hypophyseal portal blood supply -CRH & arginine vasopressin stimulates expression and release of adrenocorticotr opin (ACTH) from anterior pituitary gland -ACTH circulates through blood stream to adrenal glands, where it induces expres sion and release of glucocorticoids -HPA axis is subject to regulation from w/i CNS and from periphery -CRH is positively regulated by serotonergic, cholinergic, and catecholaminergic systems -glucocorticoids negatively feed back to suppress HPA axis at both hypothalamic and pituitary levels -other neuropeptides such as gamma-aminobutyric acid/benzodiazepines (GABA/BZD) inhibit serotonin-induced CRH secretion -glucocorticoids regulate a wide variety of immune cell expression and functions -glucocorticoids modulate cytokine expression, adhesion molecular expression, im mune cell trafficking, immune cell maturation and differentiation, expression of chemoattractants and c ell migration, and production of inflammatory mediators and other inflammatory molecules -at physiologic conc, glucocorticoids are not totally immunosuppressive, but spe cifically regulate immune response -at lower concs, glucocorticoids cause a shift in immune responses from a proinf lammatory cytokine pattern of inc interleukin (IL)-1 and tumor necrosis factor (TNF) alpha to an anti-inflamma tory cytokine pattern of inc IL-10 and IL-1 receptor antagonist -in addition to HPA axis, other central hormone systems, such as hypothalamic-pi tuitary-gonadal axis and, in particular, estrogen also modulate immune system -females of all species have greatly inc risk of developing many autoimmune/infl ammatory diseases such as systemic lupus erythematosus, rheumatoid arthritis, and mulitple sclerosis -regulation of immune system by estrogens is impt during pregnancy, where a bala nce btwn glucocorticoid and estrogen regulation plays a role in suppression of the maternal immune syste m to prevent rejection of fetus -imptce of in vivo modulation of immune sysetm by the estrogen receptor -knockout mouse models indicate that both estrogen receptors alpha and beta are impt for thymus development and atrophy in a gender-specific manner -sympathetic NS regulates immune system at a regional, local, and systemic level -immune organs, incl thymus, spleen, and lymph nodes, are innervated by sympathe tic nerves -immune cells express NT receptors (eg: adrenergic receptors on lymphocytes), wh ich allow them to respond to NT released from these nerves -diff lymphocye populations are differentially sensitive to beta-adrenergic stim ulation -systemic NE and E inhibit production of proinflammatory cytokines, such as IL-1 2, TNF alpha, and interferon gamma, and stimulate production of anti-inflammatory cytokines such a s IL-10 and transforming growth factor beta -through this mech, systemic catecholamines may cause selective suppression of c ellular immunity (Th1 responses) and enhance humoral immunity (Th2 responses) -however, in certain local responses and under certain conditions, catecholamine s may enhance regional immune responses through induction of IL-1, TNF alpha, and IL-8 production -peripheral NS regulates immunity locally, at sites of inflammation through neur opeptides, such as substance P, peripherally released CRH, and vasoactive intestinal polypeptide -these molecules are released from nerve endings/synapses or may be synthesized & released by immune cells and tend to have proinflammatory effects -opiate-mediated mechs directly affect immune responses -morphine decs mitogen responsiveness and natural killer cell
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