
doi: 10.1159/000343965
pmid: 25224888
It has been well established that there is bidirectional communication between the immune and central nervous systems. One context in which this interaction has been extensively studied is that of the stress response. Stress, whether physical or psychological, induces alterations in immune function. Often exposure to a stressor results in pro-inflammatory responses in the brain and periphery. These responses are mediated by a variety of inflammatory molecules including neuropeptides, cytokines, and stress hormones among others. Here, we will discuss several of the more comprehensively studied of these inflammatory mediators and their role(s) in stress-induced neurogenic inflammation.
Inflammation, NF-kappa B, Nitric Oxide Synthase Type II, Substance P, Nitric Oxide, Catecholamines, Cyclooxygenase 2, Animals, Cytokines, Humans, Neuropeptide Y, Nervous System Diseases, Glucocorticoids, Stress, Psychological
Inflammation, NF-kappa B, Nitric Oxide Synthase Type II, Substance P, Nitric Oxide, Catecholamines, Cyclooxygenase 2, Animals, Cytokines, Humans, Neuropeptide Y, Nervous System Diseases, Glucocorticoids, Stress, Psychological
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