TY - JOUR
T1 - Glucocorticoids alter fever and IL-6 responses to psychological stress and to lipopolysaccharide
AU - Morrow, L. E.
AU - McClellan, J. L.
AU - Conn, C. A.
AU - Kluger, M. J.
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1993
Y1 - 1993
N2 - The purpose of this study was to determine whether glucocorticoids exert inhibitory feedback on lipopolysaccharide (LPS)-induced fever, stress- induced fever (exposure to an open field), and plasma concentrations of interleukin-6 (IL-6)-like and tumor necrosis factor-α (TNF)-like activity in biotelemetered rats. Injections of LPS (50 μg/kg) or exposure to an open field (30 min) led to significantly higher fevers in adrenalectomized (ADX) rats than in sham-ADX rats. To test the hypothesis that higher fevers were specifically the result of an absence of glucocorticoids, the glucocorticoid antagonist RU 38486 (20 mg/kg) was administered orally to rats with intact adrenal glands. The RU 38486-treated rats had higher plasma concentrations of IL-6-like activity and developed significantly higher fevers than did vehicle-treated rats. Rats injected intracerebroventricularly with 10 ng RU 38486 also developed higher fevers. Other ADX animals were implanted subcutaneously with replacement corticosterone pellets before exposure to an open field or injection with LPS. In response to an open field or injection with LPS, ADX animals implanted with replacement pellets that mimic plasma concentrations of corticosterone observed in stressed animals (100-mg pellets) developed fevers that were significantly lower than those observed in ADX rats given placebo pellets, but that were not different from fevers in sham-ADX rats given placebo pellets. ADX animals implanted with replacement pellets that mimic plasma concentrations of corticosterone observed in unstressed animals (25-mg pellets) developed fevers that were significantly higher than those observed in sham-ADX rats given placebo pellets, but that were not different from fevers in ADX rats given placebo pellets. We conclude that elevated glucocorticoids exert an inhibitory feedback on LPS-induced fever, fever induced by psychological stress, and plasma concentrations of IL-6-like activity at the height of both fevers.
AB - The purpose of this study was to determine whether glucocorticoids exert inhibitory feedback on lipopolysaccharide (LPS)-induced fever, stress- induced fever (exposure to an open field), and plasma concentrations of interleukin-6 (IL-6)-like and tumor necrosis factor-α (TNF)-like activity in biotelemetered rats. Injections of LPS (50 μg/kg) or exposure to an open field (30 min) led to significantly higher fevers in adrenalectomized (ADX) rats than in sham-ADX rats. To test the hypothesis that higher fevers were specifically the result of an absence of glucocorticoids, the glucocorticoid antagonist RU 38486 (20 mg/kg) was administered orally to rats with intact adrenal glands. The RU 38486-treated rats had higher plasma concentrations of IL-6-like activity and developed significantly higher fevers than did vehicle-treated rats. Rats injected intracerebroventricularly with 10 ng RU 38486 also developed higher fevers. Other ADX animals were implanted subcutaneously with replacement corticosterone pellets before exposure to an open field or injection with LPS. In response to an open field or injection with LPS, ADX animals implanted with replacement pellets that mimic plasma concentrations of corticosterone observed in stressed animals (100-mg pellets) developed fevers that were significantly lower than those observed in ADX rats given placebo pellets, but that were not different from fevers in sham-ADX rats given placebo pellets. ADX animals implanted with replacement pellets that mimic plasma concentrations of corticosterone observed in unstressed animals (25-mg pellets) developed fevers that were significantly higher than those observed in sham-ADX rats given placebo pellets, but that were not different from fevers in ADX rats given placebo pellets. We conclude that elevated glucocorticoids exert an inhibitory feedback on LPS-induced fever, fever induced by psychological stress, and plasma concentrations of IL-6-like activity at the height of both fevers.
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U2 - 10.1152/ajpregu.1993.264.5.r1010
DO - 10.1152/ajpregu.1993.264.5.r1010
M3 - Article
C2 - 8498588
AN - SCOPUS:0027288203
VL - 264
SP - R1010-R1016
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
SN - 0363-6119
IS - 5 33-5
ER -