PMID- 9215292
OWN - NLM
STAT- MEDLINE
DCOM- 19970807
LR  - 20220408
IS  - 0021-972X (Print)
IS  - 0021-972X (Linking)
VI  - 82
IP  - 7
DP  - 1997 Jul
TI  - Exercise and circadian rhythm-induced variations in plasma cortisol 
      differentially regulate interleukin-1 beta (IL-1 beta), IL-6, and tumor necrosis 
      factor-alpha (TNF alpha) production in humans: high sensitivity of TNF alpha and 
      resistance of IL-6.
PG  - 2182-91
AB  - Although we have previously shown that the integrity of inflammatory 
      mediator-induced activation of the hypothalamic-pituitary-adrenal axis is 
      essential for conferring resistance to inflammatory disease in susceptible Lewis 
      rats, the role of endogenous glucocorticoid secretion in human immune function in 
      either health or disease is less clear. To further understand the relevance of 
      physiological variations in plasma cortisol on immune function in humans, we 
      evaluated ex vivo lipopolysaccharide-induced interleukin-1 beta (IL-1 beta), 
      IL-6, and tumor necrosis factor-alpha (TNF alpha) production in the whole blood 
      of healthy volunteers studied under conditions chosen to approximate either 
      physiological or pharmacological glucocorticoid levels. Administration of a 
      pharmacological dose of hydrocortisone suppressed the production of all three 
      cytokines, whereas administration of a physiological dose of hydrocortisone 
      suppressed only TNF alpha production. Stress-induced levels of glucocorticoids, 
      achieved during exercise at 100% maximal oxygen utilization, suppressed IL-1 beta 
      and TNF alpha production, but were without effect on IL-6 production. In 
      addition, circadian variations of cortisol were associated with decreased TNF 
      alpha production, but were without effect on IL-1 beta or IL-6 production. These 
      studies challenge the generally accepted idea that glucocorticoids consistently 
      suppress cytokine production and indicate a hierarchy of sensitivity, with TNF 
      alpha having the greatest sensitivity, IL-1 beta having intermediate sensitivity, 
      and IL-6 being resistant. The resistance of IL-6 production to glucocorticoid 
      suppression is compatible with data suggesting an antiinflammatory as well as a 
      proinflammatory action for this cytokine.
FAU - DeRijk, R
AU  - DeRijk R
AD  - Clinical Neuroendocrinology Branch, National Institute of Mental Health, National 
      Institutes of Health, Bethesda, Maryland 20892, USA. r.rijk@lacdr.leidenuniv.nl
FAU - Michelson, D
AU  - Michelson D
FAU - Karp, B
AU  - Karp B
FAU - Petrides, J
AU  - Petrides J
FAU - Galliven, E
AU  - Galliven E
FAU - Deuster, P
AU  - Deuster P
FAU - Paciotti, G
AU  - Paciotti G
FAU - Gold, P W
AU  - Gold PW
FAU - Sternberg, E M
AU  - Sternberg EM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Enterotoxins)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-2)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Superantigens)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 39424-53-8 (enterotoxin B, staphylococcal)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Adult
MH  - *Circadian Rhythm
MH  - Dose-Response Relationship, Drug
MH  - Enterotoxins/pharmacology
MH  - *Exercise
MH  - Female
MH  - Humans
MH  - Hydrocortisone/administration & dosage/*blood
MH  - Interleukin-1/*blood
MH  - Interleukin-2/blood
MH  - Interleukin-6/*blood
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - Middle Aged
MH  - Superantigens/pharmacology
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 1997/07/01 00:00
MHDA- 1997/07/01 00:01
CRDT- 1997/07/01 00:00
PHST- 1997/07/01 00:00 [pubmed]
PHST- 1997/07/01 00:01 [medline]
PHST- 1997/07/01 00:00 [entrez]
AID - 10.1210/jcem.82.7.4041 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 1997 Jul;82(7):2182-91. doi: 10.1210/jcem.82.7.4041.