INTERLEUKIN 1 (IL-1) TYPE I RECEPTORS MEDIATE ACTIVATION OF RAT HYPOTHALAMUS–PITUITARY–ADRENAL AXIS AND INTERLEUKIN 6 PRODUCTION AS SHOWN BY RECEPTOR TYPE SELECTIVE DELETION MUTANTS OF IL-1β

Major Depression and Activation of The Inflammatory Response System

“…IL-6 may stimulate the HPA-axis at concentrations known to occur in human plasma (Navarra et al, 1991) and sufficiently to exert its actions on immune cells (Carmeliet, Vankelecom, Van Damme, Billiau, & Denef, 1991). It is reported that IL-l(3-induced ACTH, corticosterone, and IL-6 production is mediated by IL-1 type I receptors (Van Dam, Malinowsky, Lenczowski, Bartfai, & Tilders, 1998). It has been shown that HPA-axis hyperactivity during IRS activation is monokine-mediated and may result from monokine-induced serotonergic and catecholaminergic turnover (Dunn, 1988;Dunn, Powell, Meitin, & Small, 1989).…”

Graves’ disease as a driver of depression: a mechanistic insight

“…IL-1 and IL-6, two proinflammatory cytokines elevated in GD ( 76 – 78 ), are typical cytokines involved in stimulating CRH/HPA axis hyperactivity. After binding to the IL-1 type I receptor, IL-1β could mediate the activation of the HPA axis in the rodent model of depression ( 79 ), which provides evidence for IL-1’s role in activating the HPA axis. As IL-1 has known effects on hypothalamic biogenic amines, the main source of corticotropin-releasing factor (CRF), it can regulate on pituitary ACTH and promote the production and release of cortisol ( 80 ), which may be the underlying mechanism of the HPA axis activation by IL-1.…”

Modalités pratiques de l'insulinothérapie en réanimation

“…Mécanismes de l'hyperglycémie À la phase aiguë d'un stress tel qu'une chirurgie, un traumatisme ou un sepsis, les hormones de contre-régulation (glucagon, cortisol, growth hormone (GH), catécholamines) sont hypersecrétées pour tenter de maintenir l'homéostasie. Les cytokines pro-inflammatoires telles que l'interleukine (IL)-1, IL-6, Tumor necrosis factor-α constituent les déterminants principaux de l'intensité de la réponse hormonale [3]. L'une des conséquences majeures de l'hyperactivité hormonale, notamment de l'augmentation des concentrations plasmatiques d'adrénaline et de cortisol, est une hyperglycémie par stimulation de la glycogénolyse et de la néoglucogenèse.…”