https://www.ncbi.nlm.nih.gov/books/NBK279017/
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The immune/inflammatory (I/I) response is influenced by the brain in a major way. This is achieved via regulation of peripheral nervous system functions and endocrine responses (1). Among other pathways the brain regulates this response through the hypothalamic-pituitary-adrenal (HPA) axis, which is activated during stress (1). On the other hand, receptors for a number of hormones, neurotransmitters and neuropeptides are carried by cells of the immune system, leading to modulation of their responses by changes in neuroendocrine and/or autonomic activity (2). Products of the I/I response, such as eicosanoids and inflammatory cytokines influence brain function. Additionally, immune cells produce a number of hormones and neuropeptides, like corticotropin-releasing hormone (CRH) and corticotropin (ACTH) which act locally as autacoids during both the early and late stages of the I/I process (3). This locally produced CRH, is subsequently called ‘peripheral CRH’.
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