PMID- 9302075
OWN - NLM
STAT- MEDLINE
DCOM- 19971023
LR  - 20061115
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 49
IP  - 5
DP  - 1997 Sep 1
TI  - Interleukin-1beta (IL-1beta)-induced modulation of the hypothalamic IL-1beta 
      system, tumor necrosis factor-alpha, and transforming growth factor-beta1 mRNAs 
      in obese (fa/fa) and lean (Fa/Fa) Zucker rats: implications to IL-1beta feedback 
      systems and cytokine-cytokine interactions.
PG  - 541-50
AB  - Interleukin-1beta (IL-1beta) induces anorexia, fever, sleep changes, and 
      neuroendocrine alterations when administered into the brain. Here, we 
      investigated the regulation of the IL-1beta system (ligand, receptors, receptor 
      accessory protein, and receptor antagonist), tumor necrosis factor-alpoha 
      (TNF-alpha), transforming growth factor (TGF)-beta1, and TGF-alpha mRNAs in the 
      hypothalamus of obese (fa/fa) and lean (Fa/Fa) Zucker rats in response to the 
      intracerebroventricular microinfusion of IL-1beta (8.0 ng/24 hr for 72 hr, a dose 
      that yields estimated pathophysiological concentrations in the cerebrospinal 
      fluid). IL-1beta increased IL-1beta, IL-1 receptor types I and II (IL-1RI and 
      IL-1RII), IL-1 receptor accessory protein soluble form (IL-1R AcP II), IL-1 
      receptor antagonist (IL-1Ra), TNF-alpha, and TGF-beta1 mRNAs in the hypothalamus 
      from obese and lean rats. IL-1beta-induced IL-1beta system and ligand (IL-1beta, 
      TNF-alpha, and TGF-beta1) mRNA profiles were highly intercorrelated in the same 
      samples. Levels of membrane-bound IL-1R AcP and TGF-alpha mRNAs did not change. 
      Heat-inactivated IL-1beta had no effect. The data suggest 1) the operation of an 
      IL-1beta feedback system (IL-1beta/IL-1RI/IL-1R Acp II/IL-1RII/IL-1Ra) and 2) 
      potential cytokine-cytokine interactions with positive (IL-1beta <--> TNF-alpha) 
      and negative (TGF-beta1 --> IL-1beta/TNF-alpha) feedback. Dysregulation of the 
      IL-1beta feedback system and the TGF-beta1/IL-1beta-TNF-alpha balance may have 
      implications for neurological disorders associated with high levels of IL-1beta 
      in the brain.
FAU - Plata-Salaman, C R
AU  - Plata-Salaman CR
AD  - Division of Molecular Biology, School of Life and Health Sciences, University of 
      Delaware, Newark 19716-2590, USA. crps@udel.edu
FAU - Ilyin, S E
AU  - Ilyin SE
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor alpha)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Animals
MH  - Feedback/*physiology
MH  - Hypothalamus/*drug effects/metabolism
MH  - Interleukin-1/*pharmacology
MH  - Male
MH  - Obesity/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Zucker
MH  - Transforming Growth Factor alpha/*drug effects/metabolism
MH  - Transforming Growth Factor beta/*metabolism
EDAT- 1997/09/25 00:00
MHDA- 2000/06/20 09:00
CRDT- 1997/09/25 00:00
PHST- 1997/09/25 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/09/25 00:00 [entrez]
AID - 10.1002/(SICI)1097-4547(19970901)49:5<541::AID-JNR4>3.0.CO;2-B [pii]
AID - 10.1002/(SICI)1097-4547(19970901)49:5<541::AID-JNR4>3.0.CO;2-B [doi]
PST - ppublish
SO  - J Neurosci Res. 1997 Sep 1;49(5):541-50. doi: 
      10.1002/(SICI)1097-4547(19970901)49:5<541::AID-JNR4>3.0.CO;2-B.