BACKGROUND Recent studies demonstrate that glucocorticoids (GCs) have both supportive (stimulatory) and suppressive effects on immune responses, depending upon the GC concentration. Since some GC effects on inflammation are stimulatory, we hypothesized that acute in vivo GC depletion would decrease inflammatory responses of human monocytes. METHODS Monocytes were isolated from healthy volunteer participants before and after in vivo treatment with; 1) IV saline, 2) IV high dose hydrocortisone (8 μg · kg−1 · min−1) followed by oral hydrocortisone overnight, and 3) oral RU486 (200 mg at 0400 and 1600 h) to block the intracellular GC receptor and IV etomidate (1.5 mg · kg−1 · h−1) for 12 h to prevent compensatory adrenal cortisol synthesis. Plasma adrenocorticotropic hormone, plasma, and salivary cortisol were measured serially. Monocytes were tested for; 1) cytokine responses, 2) expression of CD163, CD119, and CD54, and 3) mRNA levels of GC-responsive inflammatory mediators. All measurements were made with and without in vitro stimulation of monocytes by lipopolysaccharide. RESULTS Cortisol and adrenocorticotropic hormone measurements demonstrated effective manipulation of in vivo cortisol. In vivo hypercortisolemia and in vivo GC depletion had reciprocal effects on monocyte mRNA levels of 4 important GC-responsive molecules: 1) GC receptor, CD163, interleukin-10, and suppressor of the cytokine synthesis-3. Monocyte cytokine responses and protein expression were not affected by GC depletion. CD163 expression was increased by hypercortisolemia. CONCLUSIONS Short-term GC depletion affects mRNA levels of GC-responsive molecules but does not affect monocyte protein expression or cytokine responses.

1. An investigation of the mechanism of diurnal excretory rhythms has been carried out on four healthy male subjects in whom the excretory rhythms were reversed by a 12 hr. shift of the activity-sleep and lightdark schedules.2. The diurnal rhythms of water, sodium, potassium, creatinine and ketogenic steroid excretion adapted to the reversal of routine at different rates.3. It is concluded, from the dissociation of these rhythms during the reversal phase, that the ketogenic steroids are not controlling either the major variation of glomerular filtration rate or the excretory rhythms of water and sodium. 4. The potassium excretory rhythm appears to be linked with the ketogenic steroid rhythm.5. The mechanism of the diurnal rhythm of urine flow is discussed in relation to these findings.

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