PMID- 11981130
OWN - NLM
STAT- MEDLINE
DCOM- 20020816
LR  - 20151119
IS  - 0145-6008 (Print)
IS  - 0145-6008 (Linking)
VI  - 26
IP  - 4
DP  - 2002 Apr
TI  - Effects of in vitro ethanol on tumor necrosis factor-alpha production by blood 
      obtained from simian immunodeficiency virus-infected rhesus macaques.
PG  - 527-34
AB  - BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha), a product of monocytes and 
      macrophages, functions as an important proinflammatory cytokine in the host's 
      response to invading pathogens. METHODS: Because both alcohol abuse and human 
      immunodeficiency virus infection affect TNF-alpha production and are known to 
      frequently coexist, this study examined the effects of simian immunodeficiency 
      virus (SIV) infection and in vitro alcohol exposure on the lipopolysaccharide 
      (LPS)-induced TNF-alpha response in blood obtained from SIV-negative and 
      -positive animals at the asymptomatic and terminal stages of infection. RESULTS: 
      Spontaneous TNF-alpha production was undetectable or low in all groups examined. 
      LPS-induced TNF-alpha production was increased in blood obtained at the 
      asymptomatic (746 +/- 226 pg/ml) and terminal (1945 +/- 1013 pg/ml) stages, 
      compared with that from SIV-negative animals (210 +/- 28 pg/ml), whereas 
      TNF-alpha messenger RNA content did not differ in LPS-stimulated blood obtained 
      from SIV-negative, asymptomatic SIV-positive, or terminal SIV-positive animals. 
      Ethanol treatment suppressed TNF-alpha protein production in all groups, whereas 
      TNF-alpha messenger RNA levels remained unchanged in blood obtained from animals 
      not infected with SIV. CONCLUSIONS: Blood cellular elements remain responsive to 
      LPS stimulation with respect to TNF production even into the acquired 
      immunodeficiency syndrome stage of SIV disease. However, intoxicating doses of 
      alcohol suppress this response, and this may contribute to the immunocompromised 
      state of the host.
FAU - Stoltz, David A
AU  - Stoltz DA
AD  - Department of Medicine, Section of Pulmonary/Critical Care, Louisiana State 
      University Health Sciences Center, New Orleans, USA.
FAU - Nelson, Steve
AU  - Nelson S
FAU - Kolls, Jay K
AU  - Kolls JK
FAU - Zhang, Ping
AU  - Zhang P
FAU - Bohm, Rudolf P
AU  - Bohm RP
FAU - Murphey-Corb, Michael
AU  - Murphey-Corb M
FAU - Bagby, Gregory J
AU  - Bagby GJ
LA  - eng
GR  - AA05470/AA/NIAAA NIH HHS/United States
GR  - AA09803/AA/NIAAA NIH HHS/United States
GR  - AA10384/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 (Central Nervous System Depressants)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Animals
MH  - Blood/*immunology/metabolism/*virology
MH  - Central Nervous System Depressants/blood
MH  - Ethanol/*blood/pharmacology
MH  - Female
MH  - Macaca mulatta
MH  - Male
MH  - RNA, Messenger/biosynthesis
MH  - Simian Acquired Immunodeficiency Syndrome/*blood/immunology
MH  - Simian Immunodeficiency Virus/immunology/isolation & purification/*physiology
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/genetics
MH  - Up-Regulation/drug effects/immunology
EDAT- 2002/05/01 10:00
MHDA- 2002/08/17 10:01
CRDT- 2002/05/01 10:00
PHST- 2002/05/01 10:00 [pubmed]
PHST- 2002/08/17 10:01 [medline]
PHST- 2002/05/01 10:00 [entrez]
PST - ppublish
SO  - Alcohol Clin Exp Res. 2002 Apr;26(4):527-34.