Corticotropin-releasing hormone deficiency unmasks the proinflammatory effect of epinephrine
AUTOR(ES)
Karalis, Katia P.
FONTE
The National Academy of Sciences
RESUMO
Traditionally, the adrenal gland has been considered an important endocrine component of the pathway to inhibit acute inflammation via hypothalamic corticotropin-releasing hormone (CRH)-mediated secretion of glucocorticoid. Immunoreactive CRH found in inflamed tissues is a potent proinflammatory factor. Using genetic and pharmacological models of CRH deficiency, we now show that CRH deficiency unmasks a major proinflammatory effect of epinephrine secreted from the adrenal medulla. Together, epinephrine and peripheral CRH stimulate inflammation, and glucocorticoid acts as a counterbalancing force in this regard. Our findings suggest that stimulation of the acute inflammatory response should be included with the other “fight-or-flight” actions of epinephrine.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=22067Documentos Relacionados
- Impaired diurnal adrenal rhythmicity restored by constant infusion of corticotropin-releasing hormone in corticotropin-releasing hormone-deficient mice.
- Corticotropin-releasing hormone regulates IL-6 expression during inflammation
- Urocortin II mediates pro‐inflammatory effects in human colonocytes via corticotropin‐releasing hormone receptor 2α
- Glucocorticoid stimulates expression of corticotropin-releasing hormone gene in human placenta.
- Corticotropin-releasing hormone: An autocrine hormone that promotes lipogenesis in human sebocytes
