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Acute Alcohol Consumption (acute + alcohol_consumption)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Moderate Alcohol Intake in Humans Attenuates Monocyte Inflammatory Responses: Inhibition of Nuclear Regulatory Factor Kappa B and Induction of Interleukin 10

ALCOHOLISM, Issue 1 2006
Pranoti Mandrekar
Background: In contrast to the deleterious effects of chronic excessive alcohol consumption on the liver and cardiovascular system, modest alcohol intake, such as 1 to 2 drinks per day, has benefits on cardiovascular mortality. Little is known about the length of time or the amounts of alcohol consumed that may cause alterations in inflammatory cells such as monocytes that are crucial to atherosclerotic vascular disease. Here, we determine in vivo effects of acute alcohol consumption on inflammatory cytokine production and nuclear regulatory factor ,B (NF- ,B) binding in human monocytes. Methods: Human blood monocytes were isolated by plastic adherence before and after acute alcohol consumption (2 ml vodka/kg body weight). Lipopolysaccharide (LPS)- and superantigen-induced tumor necrosis factor , (TNF ,), interleukin (IL)-1,, and IL-10 production were then determined in monocytes by ELISA. Nuclear regulatory factor- ,B activity of monocytes before and after alcohol consumption was estimated by electromobility shift assay and promoter-driven reporter activity. I,B, was determined by Western blotting in the cytoplasmic extracts. Results: Eighteen hours after moderate alcohol consumption, we found a significant reduction in monocyte production of inflammatory mediators, TNF- , and IL-1,, in response to LPS or staphylococcal enterotoxin B stimulation. Acute alcohol consumption inhibited LPS-induced DNA binding of the p65/p50 NF- ,B in monocytes that regulates the expression of both the TNF- , and the IL-1, genes. Consistent with this, acute alcohol treatment (25 mM) significantly reduced LPS-induced activation of an NF- ,B-driven reporter gene suggesting inhibition of this proinflammatory signaling pathway. Further, LPS-induced I,B, degradation was not affected by acute alcohol consumption indicating an I,B, -independent mechanism, as observed earlier in the in vitro acute alcohol studies. In contrast, monocyte production of the anti-inflammatory cytokine, IL-10, was augmented by acute alcohol intake. Conclusions: Our findings suggest that acute alcohol consumption has dual anti-inflammatory effects that involve augmentation of IL-10 and attenuation of monocyte inflammatory responses involving inhibition of NF- ,B. These mechanisms may contribute to the beneficial effects of moderate alcohol use on atherosclerosis. [source]

A cross-national meta-analysis of alcohol and injury: data from the Emergency Room Collaborative Alcohol Analysis Project (ERCAAP)

ADDICTION, Issue 9 2003
Cheryl J. Cherpitel
ABSTRACT Aims, To examine the relationship of acute alcohol consumption with an injury compared to a non-injury event in the emergency room across ERs in five countries. Design, Meta-analysis was used to evaluate the consistency and magnitude of the association of a positive blood alcohol concentration (BAC) at the time of arrival in the ER and self-reported consumption within 6 hours prior to the event with admission to the ER for an injury compared to a non-injury, and the extent to which contextual (socio-cultural and organizational) variables explain effect sizes. Findings, When controlling for age, gender and drinking five or more drinks on an occasion at least monthly, pooled effect size was significant and of a similar magnitude for both BAC and self-reported consumption, with those positive on either measure over half as likely again to be admitted to the ER with an injury compared to a medical problem. Effect sizes were found to be homogeneous across ERs for BAC, but not for self-report. Trauma center status and legal level of intoxication were positively predictive of self-reported consumption effect size on injury. Conclusions, These data suggest a moderate, but robust association of a positive BAC and self-report with admission to the ER with an injury, and that contextual variables also appear to play a role in the alcohol,injury nexus. [source]

Acute Ethanol Effects on Brain Activation in Low- and High-Level Responders to Alcohol

ALCOHOLISM, Issue 7 2010
Ryan S. Trim
Background:, A low level of response (LR) to alcohol is an important endophenotype associated with an increased risk of alcoholism. However, little is known about how neural functioning may differ between individuals with low and high LRs to alcohol. This study examined whether LR group effects on neural activity varied as a function of acute alcohol consumption. Methods:, A total of 30 matched high- and low-LR pairs (N = 60 healthy young adults) were recruited from the University of California, San Diego, and administered a structured diagnostic interview and laboratory alcohol challenge followed by two functional magnetic resonance imaging (fMRI) sessions under placebo and alcohol conditions, in randomized order. Task performance and blood oxygen level-dependent response contrast to high relative to low working memory load in an event-related visual working memory (VWM) task were examined across 120 fMRI sessions. Results:, Both LR groups performed similarly on the VWM task across conditions. A significant LR group by condition interaction effect was observed in inferior frontal and cingulate regions, such that alcohol attenuated the LR group differences found under placebo (p < 0.05). The LR group by condition effect remained even after controlling for cerebral blood flow, age, and typical drinking quantity. Conclusions:, Alcohol had differential effects on brain activation for low- and high-LR individuals within frontal and cingulate regions. These findings represent an additional step in the search for physiological correlates of a low LR and identify brain regions that may be associated with the low LR response. [source]

Moderate Alcohol Intake in Humans Attenuates Monocyte Inflammatory Responses: Inhibition of Nuclear Regulatory Factor Kappa B and Induction of Interleukin 10

ALCOHOLISM, Issue 1 2006
Pranoti Mandrekar
Background: In contrast to the deleterious effects of chronic excessive alcohol consumption on the liver and cardiovascular system, modest alcohol intake, such as 1 to 2 drinks per day, has benefits on cardiovascular mortality. Little is known about the length of time or the amounts of alcohol consumed that may cause alterations in inflammatory cells such as monocytes that are crucial to atherosclerotic vascular disease. Here, we determine in vivo effects of acute alcohol consumption on inflammatory cytokine production and nuclear regulatory factor ,B (NF- ,B) binding in human monocytes. Methods: Human blood monocytes were isolated by plastic adherence before and after acute alcohol consumption (2 ml vodka/kg body weight). Lipopolysaccharide (LPS)- and superantigen-induced tumor necrosis factor , (TNF ,), interleukin (IL)-1,, and IL-10 production were then determined in monocytes by ELISA. Nuclear regulatory factor- ,B activity of monocytes before and after alcohol consumption was estimated by electromobility shift assay and promoter-driven reporter activity. I,B, was determined by Western blotting in the cytoplasmic extracts. Results: Eighteen hours after moderate alcohol consumption, we found a significant reduction in monocyte production of inflammatory mediators, TNF- , and IL-1,, in response to LPS or staphylococcal enterotoxin B stimulation. Acute alcohol consumption inhibited LPS-induced DNA binding of the p65/p50 NF- ,B in monocytes that regulates the expression of both the TNF- , and the IL-1, genes. Consistent with this, acute alcohol treatment (25 mM) significantly reduced LPS-induced activation of an NF- ,B-driven reporter gene suggesting inhibition of this proinflammatory signaling pathway. Further, LPS-induced I,B, degradation was not affected by acute alcohol consumption indicating an I,B, -independent mechanism, as observed earlier in the in vitro acute alcohol studies. In contrast, monocyte production of the anti-inflammatory cytokine, IL-10, was augmented by acute alcohol intake. Conclusions: Our findings suggest that acute alcohol consumption has dual anti-inflammatory effects that involve augmentation of IL-10 and attenuation of monocyte inflammatory responses involving inhibition of NF- ,B. These mechanisms may contribute to the beneficial effects of moderate alcohol use on atherosclerosis. [source]