It has long been known that stressful conditions can suppress immune functions, reducing the ability of an individual to recover from infection. This can be explained by the fact that the neuroendocrine and immune systems are interconnected, forming an integrated system with common mediators and receptors. Cells of the immune system have receptors for many hormones, hormone-releasing factors and neurotransmitters - evidence that these molecules regulate immune responses. Moreover, immune cells themselves produce hormones and endorphins.
The interplay between the neuroendocrine and immune systems is bi-directional, as exemplified by the control of Cortisol release from the adrenal glands during stress. Cortisol has well-known anti-inflammatory properties and it also suppresses the immune system. The signal for the release of cortisol originates in the brain. Electrical signals generated in the brain, and also IL-1 and IL-6 synthesized in brain cells, stimulate the hypothalamus to produce corticotrophin-releasing hormone (CRH), which induces the anterior lobe of the pituitary gland to release adrenocorticotrophic hormone (ACTH). CRH can also induce lymphocytes to produce their own ACTH. The ACTH is released into the bloodstream and, on reaching the target organ (adrenal glands), stimulates the adrenal cells to secrete cortisol. At excessive concentrations, ACTH inhibits the release of CRH and ACTH by negative feedback to the hypothalamus and anterior pituitary gland.
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