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Abstract
Communication between the central components of the stress response and the immune
system plays an important role in susceptibility to inflammatory disease. This communication
occurs through hormonal and neuronal mechanisms. Hormonal mechanisms involve activation
of the hypothalamic-pituitary-adrenal (HPA) axis by immune system products, e.g. cytokines.
The stimulated HPA axis regulates immune responses through the immunosuppressive effects
of glucocorticoids. Neuronal mechanisms include direct innervation of immune organs.
Cytokine activation of the HPA axis and the resultant glucocorticoid-induced suppression
of immune and inflammatory responses represent an important mechanism whereby the
central stress response modulates peripheral inflammation. Interruption of this communication
is associated with exacerbation of inflammatory disease. Conversely, intracerebroventricular
transplantation of hypothalamic tissue from inflammatory resistant rats into susceptible
rats reduces peripheral inflammation by more than 85%.