scholarly journals Acute ethanol exposure inhibits macrophage IL-6 production: role of p38 and ERK1/2 MAPK

2003 ◽  
Vol 75 (3) ◽  
pp. 553-559 ◽  
Author(s):  
Joanna Goral ◽  
Mashkoor A. Choudhry ◽  
Elizabeth J. Kovacs
Keyword(s):  
Ethanol Exposure ◽  
Acute Ethanol

scholarly journals Role of acute ethanol exposure and TLR4 in early events of sepsis in a mouse model

Alcohol ◽  
2011 ◽  
Vol 45 (8) ◽  
pp. 795-803 ◽  
Author(s):  
Minny Bhatty ◽  
Basit L. Jan ◽  
Wei Tan ◽  
Stephen B. Pruett ◽  
Bindu Nanduri
Keyword(s):  
Mouse Model ◽  
Ethanol Exposure ◽  
Acute Ethanol

scholarly journals Highlight Article: Conditioning the neuroimmune response to ethanol using taste and environmental cues in adolescent and adult rats

2019 ◽  
Vol 244 (5) ◽  
pp. 362-371
Author(s):  
Anny Gano ◽  
Ricardo M Pautassi ◽  
Tamara L Doremus-Fitzwater ◽  
Thaddeus M Barney ◽  
Andrew S Vore ◽  
...  
Keyword(s):  
Young Adults ◽  
Alcohol Abuse ◽  
Drugs Of Abuse ◽  
Ethanol Exposure ◽  
Single Trial ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Acute Ethanol ◽  
Conditioned Effects

Our work in adult Sprague-Dawley rats has shown elevation of the cytokine Interleukin (IL)-6 in the hippocampus and amygdala following acute and repeated binge-like doses of ethanol during intoxication. Previously, we have shown that in adults, the central IL-6 response to a sub-threshold dose of ethanol was sensitized by repeated pairings of ethanol as an unconditioned stimulus (US) with an odor conditioned stimulus (CS).In the present studies, acute ethanol exposure (4 g/kg intraperitoneal) was paired with a combined odor and taste cue using a single trial learning procedure, after which rats were tested for conditioned effects of the CS on neuroimmune gene expression. We found that IL-6 was significantly elevated in the amygdala based on exposure to the CS after just one CS–US pairing in young adolescent rats (age P32–40), an effect that was more modest in young adults (P72–80). These data indicate that, despite a normal disposition toward a blunted neuroimmune response to ethanol, adolescents were more sensitive than adults to forming learned associations between ethanol’s neuroimmune effects and conditioned stimuli. Given the emergent role of the immune system in alcoholism, such as regulating ethanol intake, these ethanol-induced conditioned effects on cytokine levels may contribute to our understanding of the unique attributes that make adolescence a time period of vulnerability in the development of later alcohol abuse behaviors. Impact statement A combined odor and taste cue was paired with a binge-like ethanol exposure (4 g/kg intraperitoneal) using a single-trial learning paradigm. Re-exposure to the CS alone was sufficient to evoke a conditioned Interleukin (IL)-6 elevation in the amygdala in adolescents, an effect that was not observed in young adults. This demonstrates a particular sensitivity of adolescents to alcohol-associated cues and neuroimmune learning, whereas prior work indicated that adults require multiple pairings of ethanol to the CS in order to achieve a conditioned amygdala IL-6 response. While the role of immune conditioning has been studied in other drugs of abuse, these findings highlight a previously unknown aspect of alcohol-related learning. Given the emergent importance of the neuroimmune system in alcohol abuse, these findings may be important for understanding cue-induced reinstatement of alcohol intake among problem drinkers.

Role of endotoxin in the hypermetabolic state after acute ethanol exposure

1998 ◽  
Vol 275 (6) ◽  
pp. G1252-G1258 ◽  
Author(s):  
Chantal A. Rivera ◽  
Blair U. Bradford ◽  
Vitor Seabra ◽  
Ronald G. Thurman
Keyword(s):  
Oxygen Uptake ◽  
Kupffer Cells ◽  
Ethanol Exposure ◽  
Ethanol Administration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hypermetabolic State ◽  
Acute Ethanol ◽  
Eicosanoid Release

This study investigated the role of endotoxin in the hypermetabolic state or swift increase in alcohol metabolism (SIAM) due to acute ethanol exposure. Female Sprague-Dawley rats (100–120 g) were given ethanol (5 g/kg) by gavage. Endotoxin measured in plasma from portal blood was not detectable in saline-treated controls; however, 90 min after ethanol, endotoxin was increased to 85 ± 14 pg/ml, and endotoxin clearance was diminished by ∼50%. Oxygen uptake in perfused livers was increased 48% by ethanol, and production of PGE2 by isolated Kupffer cells was increased similarly. These effects were blunted by elimination of gram-negative bacteria and endotoxin with antibiotics before ethanol administration. To reproduce ethanol-induced endotoxemia, endotoxin was infused via the mesenteric vein at a rate of 2 ng ⋅ kg−1 ⋅ h−1. Endotoxin mimicked the effect of ethanol on oxygen uptake. The specific Kupffer cell toxicant GdCl3completely prevented increases in oxygen uptake due to endotoxin. These findings demonstrate that endotoxin plays a pivotal role in SIAM, most likely by stimulating eicosanoid release from Kupffer cells.

Effects of ethanol exposure on the embryo–fetus: experimental considerations, mechanisms, and the role of prostaglandins

1991 ◽  
Vol 69 (5) ◽  
pp. 550-569 ◽  
Author(s):  
Graeme N. Smith ◽  
John Patrick ◽  
Ken R. Sinervo ◽  
James F. Brien
Keyword(s):  
Underlying Mechanism ◽  
Ethanol Exposure ◽  
Abnormal Development ◽  
Prenatal Ethanol Exposure ◽  
Critical Periods ◽  
Acute Ethanol ◽  
Tremendous Amount ◽  
Near Term ◽  
Primary Focus

The purpose of this review is to critically examine the effects of ethanol on the embryo–fetus. There has been a tremendous amount of human epidemiological and experimental animal research on the characterization of the anomalies produced by chronic prenatal ethanol exposure and the identification of critical periods of vulnerability and critical amounts of ethanol necessary to produce fetal effects and (or) abnormal development. Few studies have examined the underlying mechanism(s) of the action of ethanol, and even fewer studies have examined the effects of single-dose ethanol exposure on the embryo–fetus. In this review, the current state of knowledge of the effects of chronic use of ethanol on the embryo–fetus is summarized. The primary focus of the review is on the embryonic–fetal effects of acute ethanol exposure, with particular emphasis on the ethanol-induced suppression of fetal breathing movements, as this effect appears to be a very sensitive index of acute exposure of the near-term fetus to ethanol. Factors to be considered in the selection of experimental animals to investigate the mechanism of action of ethanol and to study the acute effects of ethanol are discussed. Postulated mechanisms of action of ethanol on the embryo–fetus are evaluated with a focus on the role of prostaglandins. Finally, future directions in this field of research are proposed.Key words: alcohol, ethanol, embryo, fetus, prostaglandins.

The role of the small GTPase Rac in macrophage phagocytosis after acute ethanol exposure

Alcohol ◽  
2009 ◽  
Vol 43 (8) ◽  
pp. 668
Author(s):  
John Karavitis ◽  
Eva L. Murdoch ◽  
Luis Ramirez ◽  
Elizabeth J. Kovacs
Keyword(s):  
Ethanol Exposure ◽  
Small Gtpase ◽  
Macrophage Phagocytosis ◽  
Acute Ethanol ◽  
Gtpase Rac
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