PMID- 10760953
OWN - NLM
STAT- MEDLINE
DCOM- 20000621
LR  - 20131121
IS  - 0730-2312 (Print)
IS  - 0730-2312 (Linking)
VI  - 77
IP  - 3
DP  - 2000 Apr
TI  - Ethanol inhibits prolactin- and tumor necrosis factor-alpha-, but not gamma 
      interferon-induced expression of intercellular adhesion molecule-1 in human 
      astrocytoma cells.
PG  - 455-64
AB  - In humans, alcohol consumption has multiple effects on the immune system. Despite 
      an increase in our understanding of the effects of alcohol on the immune system, 
      little is known about the effect of alcohol on the neuroimmune response. In the 
      central nervous system (CNS), astrocytes and microglial function as immune 
      effector cells. In response to infection of injury, astrocytes increase in number 
      and size, express several proinflammatory cytokines, MHC class I and II antigens, 
      and several adhesion molecules, including intercellular adhesion molecule-1 
      (ICAM-1). Interactions between ICAM-1 and its counter-receptors play an important 
      role in the regulation of neuroimmune response. In this study, cultured human 
      astrocytoma cells were used to examine the effect of ethanol on ICAM-1 
      expression. Western blot analyses show that quiescent astrocytes express, at 
      least, four immunoreactive ICAM-1 proteins with apparent molecular weights 55, 
      67, 82, and 90 kDa. Incubation of human astrocytoma cells with tumor necrosis 
      factor-alpha (TNF-alpha) or prolactin (PRL) resulted in marked increases in all 
      four immunoreactive ICAM-1 proteins. In the presence of ethanol, however, PRL- 
      and TNF-alpha-induced increases in all four immunoreactive ICAM-1 proteins were 
      markedly inhibited. ICAM-1 is a cell surface transmembrane glycoprotein. Using a 
      cell surface specific ICAM-1 adhesion assay we found that in human astrocytoma 
      cells TNF-alpha, interferongamma (IFN-gamma) and PRL increased cell surface 
      ICAM-1 expression. Consistent with our Western blot analyses, ethanol 
      significantly inhibited TNF-alpha- and PRL-induced cell surface ICAM-1 
      expression. By contrast, IFN-gamma-induced ICAM-1 expression was not inhibited by 
      exposure of the cells to ethanol. Expression of ICAM-1 is regulated predominantly 
      at the transcriptional level. In the present report, we show that TNF-alpha 
      increased ICAM-1 mRNA levels in human astrocytoma cells and that ethanol markedly 
      blocked TNF-alpha-induced increases in ICAM-1 mRNA levels. Further, we found that 
      PRL-induced ICAM-1 expression was, at least in part, due to a PRL-induced 
      increase in TNF-alpha syntheses and secretion. Our results clearly indicate that 
      ethanol has a pronounced effect on ICAM-1 expression in human astrocytoma cells, 
      thus suggesting that ETOH exposure may impair the immune response in the CNS by 
      blocking leukocytes adhesion and migration into the CNS in response to injury or 
      infection.
CI  - Copyright 2000 Wiley-Liss, Inc.
FAU - DeVito, W J
AU  - DeVito WJ
AD  - Division of Endocrinology, University of Massachusetts Medical Center, Worcester, 
      Massachusetts 01655, USA.
FAU - Stone, S
AU  - Stone S
FAU - Mori, K
AU  - Mori K
FAU - Shamgochian, M
AU  - Shamgochian M
LA  - eng
GR  - AA11277/AA/NIAAA NIH HHS/United States
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 Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Central Nervous System Depressants)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 3K9958V90M (Ethanol)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9002-62-4 (Prolactin)
SB  - IM
MH  - Animals
MH  - Astrocytoma/*metabolism
MH  - Blotting, Northern
MH  - Blotting, Western
MH  - Cell Adhesion
MH  - Central Nervous System Depressants/*pharmacology
MH  - Dose-Response Relationship, Drug
MH  - Ethanol/*pharmacology
MH  - Fibrosarcoma/metabolism
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*biosynthesis
MH  - Interferon-gamma/*pharmacology
MH  - Mice
MH  - Prolactin/*antagonists & inhibitors
MH  - RNA, Messenger/metabolism
MH  - Recombinant Proteins/metabolism
MH  - Time Factors
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
EDAT- 2000/04/13 09:00
MHDA- 2000/06/24 11:00
CRDT- 2000/04/13 09:00
PHST- 2000/04/13 09:00 [pubmed]
PHST- 2000/06/24 11:00 [medline]
PHST- 2000/04/13 09:00 [entrez]
AID - 10.1002/(SICI)1097-4644(20000601)77:3<455::AID-JCB10>3.0.CO;2-S [pii]
PST - ppublish
SO  - J Cell Biochem. 2000 Apr;77(3):455-64.