PMID- 7943653
OWN - NLM
STAT- MEDLINE
DCOM- 19941024
LR  - 20190825
IS  - 0145-6008 (Print)
IS  - 0145-6008 (Linking)
VI  - 18
IP  - 3
DP  - 1994 Jun
TI  - Regulatory potential of ethanol and retinoic acid on human monocyte functions.
PG  - 548-54
AB  - Retinoic acid (RA), a metabolic product of vitamin A, has been shown to affect a 
      variety of immune functions, including monocytes. Monocyte functions and mediator 
      production are also modulated by ethanol exposure. This study demonstrates that 
      therapeutic doses of RA (0.1-10 microM) significantly increase transforming 
      growth factor-beta (TGF beta) production both in THP-1, human myelomonocytic 
      cells, and in human peripheral blood monocytes. We have previously reported TGF 
      beta induction by ethanol in human M theta. Combination of RA stimulation with 
      acute in vitro ethanol treatment, however, resulted in significantly lower M 
      theta TGF beta production than TGF beta levels induced by RA alone (p < 0.003). 
      Down-regulation of M theta TGF beta production by ethanol was tested at the 
      concentration range of 25-150 mM and occurred both at high and low RA 
      concentrations (10-0.1 microM). In contrast to its inhibitory effect on 
      RA-induced M theta TGF beta production, ethanol augmented TGF beta production 
      induced by muramyl dipeptide (20 micrograms/ml), suggesting that ethanol can 
      either up- or down-regulate M theta TGF beta production, depending on the 
      costimulatory factors. RA also induced a moderate increase in M theta tumor 
      necrosis factor-alpha (TNF alpha) production, which was down-regulated by ethanol 
      both at the level of secreted and cell-associated TNF alpha. In addition to 
      regulation of cytokine production, both RA and ethanol decreased expression of 
      CD4 on THP-1 cells. The degree of inhibition of CD4 expression by RA was more 
      significant than by ethanol, but RA-induced decrease in CD4 expression was not 
      significantly affected by the combined stimulation with ethanol.(ABSTRACT 
      TRUNCATED AT 250 WORDS)
FAU - Szabo, G
AU  - Szabo G
AD  - Department of Surgery, University of Massachusetts Medical Center, Worcester 
      01655.
FAU - Puppolo, M
AU  - Puppolo M
FAU - Verma, B
AU  - Verma B
FAU - Catalano, D
AU  - Catalano D
LA  - eng
GR  - AA 08577/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  - England
TA  - Alcohol Clin Exp Res
JT  - Alcoholism, clinical and experimental research
JID - 7707242
RN  - 0 (CD4 Antigens)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 3K9958V90M (Ethanol)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - CD4 Antigens/*metabolism
MH  - Cell Line
MH  - Dose-Response Relationship, Drug
MH  - Ethanol/*toxicity
MH  - Humans
MH  - Immune Tolerance/drug effects/immunology
MH  - Monocytes/*drug effects/immunology
MH  - Transforming Growth Factor beta/*metabolism
MH  - Tretinoin/*pharmacology
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 1994/06/01 00:00
MHDA- 1994/06/01 00:01
CRDT- 1994/06/01 00:00
PHST- 1994/06/01 00:00 [pubmed]
PHST- 1994/06/01 00:01 [medline]
PHST- 1994/06/01 00:00 [entrez]
AID - 10.1111/j.1530-0277.1994.tb00908.x [doi]
PST - ppublish
SO  - Alcohol Clin Exp Res. 1994 Jun;18(3):548-54. doi: 
      10.1111/j.1530-0277.1994.tb00908.x.