PMID- 9011765
OWN - NLM
STAT- MEDLINE
DCOM- 19970206
LR  - 20190826
IS  - 0169-328X (Print)
IS  - 0169-328X (Linking)
VI  - 36
IP  - 1
DP  - 1996 Feb
TI  - Adrenalectomy enhances pro-inflammatory cytokines gene expression, in the spleen, 
      pituitary and brain of mice in response to lipopolysaccharide.
PG  - 53-62
AB  - To assess the possible influence of endogenous glucocorticoids on cytokine 
      expression in the brain, adrenalectomized mice and sham operated mice were 
      injected with saline or lipopolysaccharide (LPS, 10 micrograms/mouse, 
      subcutaneously) and the levels of transcripts for IL-1 alpha, IL-1 beta, IL-1ra, 
      IL-6 and tumor necrosis factor-alpha (TNF alpha) were determined 2 h after 
      treatment in the spleen, pituitary, hypothalamus, hippocampus and striatum, using 
      semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). 
      Levels of IL-1 beta were measured by ELISA in plasma and tissues of mice 
      sacrificed after the administration of LPS or saline. LPS induced the expression 
      of pro-inflammatory cytokines at the mRNA level in all tissues under 
      investigation, except for TNF alpha in the hippocampus. This effect was 
      potentiated by adrenalectomy in the spleen for IL-1 alpha and IL-1ra, the 
      pituitary for cytokines other than IL-1ra, the hypothalamus for all cytokines, 
      the hippocampus for cytokines other than TNF alpha, and the striatum for IL-1 
      alpha and IL-6. In saline-treated mice, adrenalectomy increased IL-1 alpha and 
      IL-1 beta gene expression in the hypothalamus and IL-1 alpha gene expression in 
      the hippocampus and striatum. LPS increased plasma and tissue levels of IL-1 
      beta, as determined by ELISA, and this effect was potentiated by adrenalectomy in 
      plasma and tissues other than the spleen. These results can be interpreted to 
      suggest that endogenous glucocorticoids regulate the neural components of the 
      host response to infection and inflammation by inhibiting cytokine expression in 
      peripheral organs and the brain.
FAU - Goujon, E
AU  - Goujon E
AD  - INRA-INSERM U394, Bordeaux, France.
FAU - Parnet, P
AU  - Parnet P
FAU - Laye, S
AU  - Laye S
FAU - Combe, C
AU  - Combe C
FAU - Dantzer, R
AU  - Dantzer R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res Mol Brain Res
JT  - Brain research. Molecular brain research
JID - 8908640
RN  - 0 (Cytokines)
RN  - 0 (Interleukins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Adrenal Glands/*physiology
MH  - Adrenalectomy
MH  - Animals
MH  - Base Sequence
MH  - Brain/*drug effects/metabolism
MH  - Corticosterone/blood
MH  - Cytokines/*genetics
MH  - Gene Expression Regulation/*drug effects
MH  - Inflammation/metabolism
MH  - Interleukins/genetics
MH  - Lipopolysaccharides/pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Molecular Sequence Data
MH  - Pituitary Gland/*drug effects/metabolism
MH  - Spleen/*drug effects/metabolism
MH  - Tumor Necrosis Factor-alpha/genetics
EDAT- 1996/02/01 00:00
MHDA- 1996/02/01 00:01
CRDT- 1996/02/01 00:00
PHST- 1996/02/01 00:00 [pubmed]
PHST- 1996/02/01 00:01 [medline]
PHST- 1996/02/01 00:00 [entrez]
AID - 0169328X9500242K [pii]
AID - 10.1016/0169-328x(95)00242-k [doi]
PST - ppublish
SO  - Brain Res Mol Brain Res. 1996 Feb;36(1):53-62. doi: 10.1016/0169-328x(95)00242-k.