title: A possible change process of inflammatory cytokines in the prolonged chronic stress and its ultimate implications for health.
abstract: Sustained stress triggers series of changes in the brain and the body. At the early stage of stress, the activated hypothalamus-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) axis can upregulate the levels of glucocorticoid (GCs) and catecholamines (CAs), respectively, and then they in turn inhibit the secretion of proinflammatory cytokines directly or indirectly while promoting the secretion of anti-inflammatory cytokines. At the prolonged stage, the sustained activated HPA demonstrates cortisol-resistance. At the same time, the inflammation related transcription pathway, such as nuclear-factor kappa-B (NF-κB) signaling, may be inhibited. Additionally, the inflammatory cytokines mediate a negative feedback regulation on themselves. Collectively, these regulations may increase the proinflammatory cytokines while decreasing the anti-inflammatory cytokines. This may further activate NF-κB and increase the proinflammation cytokines, which in turn reduce the inflammatory responses, contributing to various diseases.
authors.affiliation: Department of Psychology, Zhejiang Sci-Tech University, 579 Mailbox, Hangzhou 310018, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Tian
authors.affiliation: Department of Psychology, Zhejiang Sci-Tech University, 579 Mailbox, Hangzhou 310018, China.
authors.forename: Gonglin
authors.initials: G
authors.lastname: Hou
authors.affiliation: Department of Psychology, Zhejiang Sci-Tech University, 579 Mailbox, Hangzhou 310018, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Li
authors.affiliation: Department of Psychology, Nanjing Normal University, Nanjing 210097, China.
authors.forename: Ti-Fei
authors.initials: TF
authors.lastname: Yuan
mesh_terms: D000818:Animals; D002908:Chronic Disease; D016207:Cytokines / Q000096:biosynthesis; D006304:Health Status; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D013315:Stress, Psychological / Q000175:diagnosis / Q000378:metabolism* / Q000523:psychology; D013997:Time Factors
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators