PMID- 8906613
OWN - NLM
STAT- MEDLINE
DCOM- 19970513
LR  - 20181113
IS  - 0895-8696 (Print)
IS  - 0895-8696 (Linking)
VI  - 7
IP  - 3
DP  - 1996 Fall
TI  - Regulation of brain interleukin-1 beta (IL-1 beta) system mRNAs in response to 
      pathophysiological concentrations of IL-1 beta in the cerebrospinal fluid.
PG  - 169-81
AB  - Interleukin-1 beta (IL-1 beta) is released during pathophysiological processes. 
      IL-1 beta induces neurological manifestations when administered into the 
      cerebrospinal fluid (CSF) at pathophysiological concentrations detected during 
      central nervous system (CNS) infections and other neurological disorders. In the 
      present study, we investigated the regulation of the IL-1 beta system in the CNS 
      in response to the chronic intracerebroventricular (icv) microinfusion of IL-1 
      beta at estimated pathophysiological concentrations in the CSF. IL-1 receptor 
      type I (IL-1RI), IL-1 receptor antagonist (IL-1Ra), and IL-1 beta mRNAs were 
      determined by sensitive RNase protection assays in brain target regions for IL-1 
      beta (cerebellum, parieto-frontal cortex, hippocampus, and midbrain). The results 
      show that chronic icy microinfusion of IL-1 beta induced significant anorexia, 
      increased the cerebellar IL-1RI mRNA content, increased IL-1Ra and IL-1 beta 
      mRNAs levels in the cerebellum > midbrain > cortex > hippocampus, and induced 
      profiles of IL-1RI mRNA, IL-1Ra mRNA, and IL-1 beta mRNA that were highly 
      intercorrelated. On the other hand, levels of rat glyceraldehyde 3-phosphate 
      dehydrogenase mRNA and 18S rRNA were fairly constant, and heat-inactivated IL-1 
      beta had no effect on food intake or on IL-1RI, IL-1Ra, and IL-1 beta mRNAs 
      levels in any brain region. The data suggest the operation of an IL-1 beta 
      feedback system (IL-1 beta/ IL-1Ra/IL-1RI) in brain regions. Dysregulation of the 
      CNS IL-1 beta feedback system may have pathophysiological significance. This may 
      be reflected, for example, in the pathogenicity and severity of neurological 
      diseases, such as CNS infections.
FAU - Ilyin, S E
AU  - Ilyin SE
AD  - School of Life and Health Sciences, University of Delaware, Newark 19716, USA.
FAU - Sonti, G
AU  - Sonti G
FAU - Gayle, D
AU  - Gayle D
FAU - Plata-Salaman, C R
AU  - Plata-Salaman CR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (IL1RN protein, human)
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Sialoglycoproteins)
SB  - IM
MH  - Animals
MH  - Brain/immunology/*metabolism
MH  - Cerebral Ventricles/*physiology
MH  - Gene Expression Regulation
MH  - Humans
MH  - Infusions, Parenteral
MH  - Interleukin 1 Receptor Antagonist Protein
MH  - Interleukin-1/*biosynthesis/*cerebrospinal fluid/pharmacology
MH  - Male
MH  - RNA, Messenger/*biosynthesis
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Interleukin-1/antagonists & inhibitors/*biosynthesis
MH  - Recombinant Proteins/biosynthesis/cerebrospinal fluid/pharmacology
MH  - Sialoglycoproteins/biosynthesis
MH  - *Transcription, Genetic
EDAT- 1996/10/01 00:00
MHDA- 1996/10/01 00:01
CRDT- 1996/10/01 00:00
PHST- 1996/10/01 00:00 [pubmed]
PHST- 1996/10/01 00:01 [medline]
PHST- 1996/10/01 00:00 [entrez]
AID - 10.1007/BF02736838 [doi]
PST - ppublish
SO  - J Mol Neurosci. 1996 Fall;7(3):169-81. doi: 10.1007/BF02736838.