Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of interleukin-18 (IL-18), a putative member of the IL-1 family, were investigated on basal and stimulated release of corticotropin-releasing hormone (CRH) and prostanoids from rat hypothalamic explants and glial cells in vitro. We found that IL-18 decreases basal and KCl-stimulated CRH release from the hypothalamus. IL-18 also reduced CRH gene expression after 1- and 3-h incubation. The cytokine did not modify basal PGE2 production by hypothalamic explants but abolished production stimulated by IL-1beta. Similar effects were also observed on cultured glial cells. The present findings show that IL-18 possesses a profile of in vitro neuroendocrine activities opposing to, and even antagonizing, those of IL-1beta.
 ...
PMID:Interleukin-18 displays effects opposite to those of interleukin-1 in the regulation of neuroendocrine stress axis. 1571 Apr 58

Corticotropin releasing hormone (CRH) is a major regulator of the stress response. This study examined whether CRH regulates interleukin-18 expression on microglia, BV2. Our data show that CRH enhanced IL-18 expression and significantly induced the secretion of functional IL-18 protein. Furthermore, CRH induced IL-18 production could be blocked by N-acetyl-L-cystein (NAC), which suggests that reactive oxygen intermediates (ROI) may be involved in regulating IL-18. Indeed, it was also found that CRH increased the generation of ROI. Taken together, these results indicate that CRH is an important mediator that regulates IL-18 expression in the brain during stress.
 ...
PMID:Regulation of IL-18 expression by CRH in mouse microglial cells. 1586 Feb 30

Psychological/physical stresses are known to cause relapses of autoimmune and inflammatory diseases. To reveal a mechanism by which noninflammatory stresses affect host defenses, responses to immobilization stress in mice were investigated, focusing on the role of a multifunctional cytokine, interleukin-18 (IL-18). In the adrenal cortex, the stress induced IL-18 precursor proteins (pro-IL-18) via adrenocorticotropic hormone (ACTH) and a superoxide-mediated caspase-1 activation pathway, resulting in conversion of pro-IL-18 to the mature form, which was released into plasma. Inhibitors of caspase-1, reactive oxygen species, and P38 mitogen-activated protein kinase (MAPK) suppressed stress-induced accumulation of plasma IL-18. These inhibitors also blocked stress-induced IL-6 expression. This, together with the observation that IL-6 was not induced in IL-18-deficient mice, showed that IL-6 induction by stress is dependent on IL-18. In stressed organisms, IL-18 may influence pathological and physiological processes. Controlling the caspase-1 activating pathway to suppress IL-18 levels may provide preventative means against stress-related disruption of host defenses.
 ...
PMID:A stress-induced, superoxide-mediated caspase-1 activation pathway causes plasma IL-18 upregulation. 1596 82