Hydrocortisone Regulation of Interleukin-6 Protein Production by a Purified Population of Human Peripheral Blood Monocytes

Breuninger, Lisa M.; Dempsey, Walla L.; Uhl, Joanne; Murasko, Donna M.

doi:10.1006/clin.1993.1171

Cited by 56 publications

(32 citation statements)

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“…Dexamethasone suppressed release of IL-6 in a dose-dependent manner, in concordance with earlier studies. 14,15 Dexamethasone stimulated leptin secretion by adipocytes in agreement with earlier studies as well. 16,17 Both effects of dexamethasone were inhibited in the presence of RU486, suggesting that they were mediated via the glucocorticoid receptor.…”

Section: Discussionsupporting

confidence: 90%

Hormonal regulation of interleukin-6 production in human adipocytes

et al. 2002

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OBJECTIVE:To elucidate the hormonal regulation of interleukin-6 (IL-6) production by human adipose tissue and its relation to leptin. DESIGN: In vitro study. Human adipocytes were incubated with dexamethasone (with or without RU486), norepinephrine and epinephrine (with or without propranolol), or insulin. MEASUREMENTS: IL-6 and leptin secretion by human adipocytes. RESULTS: A gradual increase in IL-6 secretion by adipocytes during differentiation was observed. A positive correlation was found between basal IL-6 release and both glycerol 3-phosphate dehydrogenase activity -a marker of adipocyte differentiation -and leptin release. Dexamethasone decreased IL-6 secretion and increased leptin secretion in a dose-dependent manner. Both catecholamines increased IL-6 and leptin secretion. The effects of dexamethasone and catecholamines on IL-6 and leptin were abrogated by RU486 and propranolol, respectively. Incubation with insulin resulted in a dose-dependent stimulation of IL-6 and leptin secretion. CONCLUSION: IL-6 is produced by human adipocytes and is a potential marker of adipocyte differentiation. Furthermore it is a hormonally regulated cytokine, suppressed by glucocorticoids, and stimulated by catecholamines and insulin in physiological concentrations.

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Section: Discussionsupporting

confidence: 90%

Hormonal regulation of interleukin-6 production in human adipocytes

et al. 2002

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“…GCs inXuence the cells of innate immunity such as monocytes/macrophages, neutrophils and NK cells (Schmidt et al, 1999), down-regulate monocyte-secreted proinXammatory mediators (Joyce et al, 1997;Breuninger et al, 1993) and inhibit adherence, chemotaxis, phagocytosis and cytotoxic activity (McGillen and Phair, 1979;Roth and Kaeberle, 1981;McEwen et al, 1997;Rogers et al, 1999). In addition, after in vivo or in vitro exposures to GCs, bactericidal and fungicidal ability (Rinehart et al, 1975), cytokine production, MHC class II expression (Snyder and Unanue, 1982) and tumoricidal activity (Hogan and Vogel, 1988;Keil et al, 1995) of humans and murine macrophages were decreased.…”

Section: Introductionmentioning

confidence: 99%

Peritoneal cavity phagocytes from the teleost sea bass express a glucocorticoid receptor (cloned and sequenced) involved in genomic modulation of the in vitro chemiluminescence response to zymosan

Vizzini

Vazzana

Cammarata

et al. 2007

General and Comparative Endocrinology

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“…Cytokines, which are released from activated immune cells after contact with invading pathogens, are the major response modifiers of immune functions. So far, only a few studies have addressed the role of cortisol in spontaneous or induced cytokine release and the reported results remain controversial [14][15][16][17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

Endogenous cortisol determines the circadian rhythm of lipopolysaccharide‐ but not lipoteichoic acid‐inducible cytokine release

et al. 2006

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To investigate the circadian rhythm of inducible cytokine release and a potential pacemaker role of endogenous cortisol, cortisol levels as well as cytokine release from ex vivo LPS-stimulated blood were assessed at 4-h intervals over 24 h in 11 volunteers. We found a significant diurnal variation for IFN-c and IL-8, and a tendency for TNF, all inversely correlated to the serum cortisol levels, but no evidence for such a rhythm for IL-1b and IL-6. In vitro IC 50 values for cytokine inhibition by hydrocortisone (HC) corresponded to the observed rank order for circadian rhythmicity. mRNA analyses revealed that this was due to a reduction of gene transcription. These effects of HC were significantly reversed by the glucocorticoid receptor antagonist RU486. Supplementation of HC in vivo to maintain morning cortisol levels throughout the day blunted the circadian rhythm of ex vivo LPS-induced cytokines. Surprisingly, no significant diurnal variation for any investigated cytokine was found in the same volunteer group upon stimulation with lipoteichoic acid (LTA), the gram-positive counterpart to LPS. Furthermore, 10-50-fold higher HC concentrations as compared to LPS were required to block LTA-induced cytokine release. LTA, in contrast to LPS, failed to activate Jun kinase, a reported target for HC action.

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Hydrocortisone Regulation of Interleukin-6 Protein Production by a Purified Population of Human Peripheral Blood Monocytes

Cited by 56 publications

References 0 publications

Hormonal regulation of interleukin-6 production in human adipocytes

Hormonal regulation of interleukin-6 production in human adipocytes

Peritoneal cavity phagocytes from the teleost sea bass express a glucocorticoid receptor (cloned and sequenced) involved in genomic modulation of the in vitro chemiluminescence response to zymosan

Endogenous cortisol determines the circadian rhythm of lipopolysaccharide‐ but not lipoteichoic acid‐inducible cytokine release

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