Interleukin 1 stimulation of the hypothalamic-pituitary-adrenal axis

Abstract

The effect of varying doses of purified human interleukin 1 (IL-1) on rectal temperature (Tr), hypothalamic corticotropin-releasing hormone (CRH), pituitary and plasma adrenocorticotropic hormone (ACTH), and plamsa corticosterone was examined in intact male rats at 24 degrees C; plasma ACTH and corticosterone responses were also studied in hypophysectomized rats. In addition, IL-1-induced changes in corticosterone concentration were investigated by means of adrenal organ cultures. Tr was measured with thermocouples. CRH and ACTH levels were determined by radioimmunoassay, and corticosterone by protein-binding assay. Intravenous administration of IL-1 (0.063-1.0 ng) resulted in hyperthermia, which began 20 min postinjection and continued for an additional 30 min. IL-1 at a dose of 0.5 ng resulted in no change in hypothalamic CRH, pituitary ACTH, or plasma ACTH levels compared with saline-treated rats. Plasma corticosterone was significantly (P less than 0.05) elevated 30 min after IL-1 administration and returned to control levels after 1 h. The higher dose of IL-1 (1.0 ng) did not affect hypothalamic CRH content, but pituitary ACTH began to rise at 15 min and was significantly (P less than 0.05) elevated 30 min after injection. Rats receiving this dose displayed elevated (P less than 0.05) plasma ACTH and corticosterone levels 30 and 60 min postinjection. No change in plasma corticosterone was observed in hypophysectomized rats administered either 1 ng of IL-1 or 1 microgram of recombinant IL-1 beta (rIL-1 beta); adrenal organ cultures treated with IL-1 (10(-11) M) responded similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

Intraamniotic interleukin-1 accelerates surfactant protein synthesis in fetal rabbits and improves lung stability after premature birth.

“…It can be envisaged that IL-1 increases the production of ACTH-releasing hormone and glucocorticoids by the fetus (50). Activation of the hypothalamic-pituitary-adrenal axis by IL-1 has been shown to occur in newborn animals (51).…”

Brown fat UCP1 is not involved in the febrile and thermogenic responses to IL-1β in mice

“…uncoupling protein-1; oxygen consumption; body temperature; knockout mouse; interleukin-1␤ PROINFLAMMATORY CYTOKINES, such as interleukin (IL)-1␤ released by activated immune cells during the host response to infection or inflammation, have potent effects on the brain. When administrated systemically or directly into the brain, these cytokines induce symptoms of illness, including fever, activation of hypothalamic-pituitary-adrenal axis, anorexia, and depressed behavior (3,7,12,17,26). Similar effects are observed when endogenous cytokines are released in response to administration of lipopolysaccharide (LPS) from gramnegative bacteria.…”

Type I Diabetes and the Role of Inflammatory-Related Cellular Signaling

“…Circulating increases in TNF- and IL-1 can stimulate the pituitary-adrenal axis to increase secretion of corticosterone (Gwosdow, Kumar et al 1990;Hall-Angeras, Angeras et al 1990). Insulinopenia, together with increased glucocorticoids have been shown to enhance muscle protein degradation through increased ubiquitin conjugation to proteins, proteolytic activity, and ubiquitin pathway component mRNA transcription (Price, Bailey et al 1996;Bailey, Wang et al 1999).…”

“…IL-1 , on the other hand increased muscle proteolysis independently of glucocorticoid inhibition Zamir, Hasselgren et al 1993). Therefore, it was determined from these studies that TNF-increased muscle proteolysis by stimulating the adrenal axis to increase release of glucocorticoids, while IL-1 can stimulate glucocorticoid release and signal muscle proteolysis independently of the mechanism of glucocorticoids (Gwosdow, Kumar et al 1990;Hall-Angeras, Angeras et al 1990). TNF-is an important pro-inflammatory cytokine for understanding T1DM-associated skeletal muscle wasting because it can activate also apoptotic signaling pathways.…”