PMID- 8865966
OWN - NLM
STAT- MEDLINE
DCOM- 19970206
LR  - 20190826
IS  - 0145-6008 (Print)
IS  - 0145-6008 (Linking)
VI  - 20
IP  - 5
DP  - 1996 Aug
TI  - Regulation of human monocyte functions by acute ethanol treatment: decreased 
      tumor necrosis factor-alpha, interleukin-1 beta and elevated interleukin-10, and 
      transforming growth factor-beta production.
PG  - 900-7
AB  - We and others have previously shown that even acute ethanol exposure has the 
      capacity to modulate immune functions, particularly monocyte functions. Herein, 
      we tested the hypothesis that acute ethanol treatment inhibits inflammatory, 
      while increasing inhibitory cytokine production in human blood monocytes that, in 
      turn, could contribute to the overall immune abnormalities seen after alcohol 
      use. Our data show that in vitro treatment of blood monocytes with a 
      physiologically relevant dose of alcohol (25 mM) results in significantly 
      decreased induction of tumor necrosis factor-alpha (TNF alpha) and interleukin 
      (IL)-1 beta by bacterial stimulation of either Gram-positive [staphylococcal 
      enterotoxin B (SEB), 1 microgram/ml of SEB] or Gram-negative [lipopolysaccharide 
      (LPS), 1 microgram/ml of LPS] origin both at the protein and mRNA levels. In 
      contrast, acute ethanol treatment induces monocyte production of mediators with 
      immunoinhibitory potential, including transforming growth factor-beta and IL-10. 
      We further show that ethanol not only induces monocyte/macrophage (Mo) IL-10 and 
      transforming growth factor-beta, but even augments bacterial (both LPS and SEB) 
      stimulation-induced production of both of these cytokines. IL-10 is a potent 
      inhibitor of Mo TNF alpha production. We found that ethanol-induced elevation in 
      Mo IL-10 levels contributes to the decreased Mo TNF alpha production to bacterial 
      challenge in ethanol-exposed Mo. However, mRNA levels for TNF alpha are 
      downregulated as early as 1.5 hr after ethanol treatment, suggesting that ethanol 
      likely has an IL-10 independent, direct effect on early signaling events of TNF 
      alpha induction.
FAU - Szabo, G
AU  - Szabo G
AD  - Department of Medicine, University of Massachusetts Medical Center, Worcester 
      01655, USA.
FAU - Mandrekar, P
AU  - Mandrekar P
FAU - Girouard, L
AU  - Girouard L
FAU - Catalano, D
AU  - Catalano D
LA  - eng
GR  - AA08577/AA/NIAAA NIH HHS/United States
GR  - AA09076/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Alcohol Clin Exp Res
JT  - Alcoholism, clinical and experimental research
JID - 7707242
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Adult
MH  - Alcoholic Intoxication/*immunology
MH  - Dose-Response Relationship, Drug
MH  - Escherichia coli/immunology
MH  - Ethanol/pharmacokinetics/*toxicity
MH  - Female
MH  - Humans
MH  - In Vitro Techniques
MH  - Interleukin-1/*blood
MH  - Interleukin-10/*blood
MH  - Lipopolysaccharides/immunology
MH  - Macrophages/drug effects/immunology
MH  - Male
MH  - Middle Aged
MH  - Monocytes/*drug effects/immunology
MH  - Transforming Growth Factor beta/*blood
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 1996/08/01 00:00
MHDA- 1996/08/01 00:01
CRDT- 1996/08/01 00:00
PHST- 1996/08/01 00:00 [pubmed]
PHST- 1996/08/01 00:01 [medline]
PHST- 1996/08/01 00:00 [entrez]
AID - 10.1111/j.1530-0277.1996.tb05269.x [doi]
PST - ppublish
SO  - Alcohol Clin Exp Res. 1996 Aug;20(5):900-7. doi: 
      10.1111/j.1530-0277.1996.tb05269.x.