Cytokine Changes following Acute Ethanol Intoxication in Healthy Men: A Crossover Study

Skulberg, A; Skulberg, Knut Ragnvald; Aass, Hans Christian Dalsbotten; Bramness, Jørgen G.

doi:10.1155/2016/3758590

Cited by 40 publications

(35 citation statements)

References 28 publications

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“…When the effect of acute high‐dose alcohol consumption on blood levels of cytokines was evaluated in alcohol‐experienced healthy male adult volunteers (vodka, 4.28 ml/kg), serum levels of IL‐1Ra were found to be elevated and the levels of the chemokine MCP‐1 decreased acutely followed by a sustained elevation levels of MCP‐1, even blood alcohol level had returned to nondetectable levels (Neupane et al, ). Taken together, these findings indicate that, in the adult, multiple cycles of alcohol exposure (Marshall et al, ; Zhao et al, ) and/or prior EtOH exposure can produce long‐lasting increases in the expression of neuroimmune genes, microglial activation, and elevated levels of serum cytokines (Crews and Vetreno, ; Zou and Crews, ).…”

Section: Discussionmentioning

confidence: 99%

“…However, clinical and experimental data suggest that alcohol may be an immunomodulatory agent (Afshar et al, ; Szabo and Mandrekar, ). Alcohol exposure can impact systemic and brain innate immune signaling leading to activation of pro‐inflammatory cytokine pathways (Szabo and Saha, ), variation in serum cytokine levels (Gonzalez‐Quintela et al, ; Neupane et al, ), and induction of neuroinflammation (Crews et al, ; Crews et al, ; de Timary et al, ; Qin et al, ).…”

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confidence: 99%

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Time Course of Blood and Brain Cytokine/Chemokine Levels Following Adolescent Alcohol Exposure and Withdrawal in Rats

Sanchez‐Alavez

Nguyen

Mori

et al. 2019

Alcoholism Clin & Exp Res

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Background: Adolescence is a critical period for neural development, and alcohol exposure during adolescence can lead to an elevated risk for health consequences as well as alcohol use disorders. Clinical and experimental data suggest that chronic alcohol exposure may produce immunomodulatory effects that can lead to the activation of pro-inflammatory cytokine pathways as well as microglial markers. The present study evaluated, in brain and blood, the effects of adolescent alcohol exposure and withdrawal on microglia and on the most representative pro-and anti-inflammatory cytokines and major chemokines that can contribute to the establishing of a neuroinflammatory environment.Methods: Wistar rats (males, n = 96) were exposed to ethanol (EtOH) vapors, or air control, for 5 weeks over adolescence (PD22-PD58). Brains and blood samples were collected at 3 time points: (i) after 35 days of vapor/air exposure (PD58); (ii) after 1 day of withdrawal (PD59), and (iii) 28 days after withdrawal (PD86). The ionized calcium-binding adapter molecule 1 (Iba-1) was used to index microglial activation, and cytokine/chemokine responses were analyzed using magnetic bead panels.Results: After 35 days of adolescent vapor exposure, a significant increase in Iba-1 immunoreactivity was seen in amygdala, frontal cortex, hippocampus, and substantia nigra. However, Iba-1 density returned to control levels at both 1 day and 28 days of withdrawal except in the hippocampus where Iba-1 density was significantly lower than controls. In serum, adolescent EtOH exposure induced a reduction in IL-13 and an increase in fractalkine at day 35. After 1 day of withdrawal, IL-18 was reduced, and IP-10 was elevated, whereas both IP-10 and IL-10 were elevated at 28 days following withdrawal. In the frontal cortex, adolescent EtOH exposure induced an increase in IL-1b at day 35, and 28 days of withdrawal, and IL-10 was increased after 28 days of withdrawal.Conclusion: These data demonstrate that EtOH exposure during adolescence produces significant microglial activation; however, inflammatory markers seen in the blood appear to differ from those observed in the brain.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Time Course of Blood and Brain Cytokine/Chemokine Levels Following Adolescent Alcohol Exposure and Withdrawal in Rats

Sanchez‐Alavez

Nguyen

Mori

et al. 2019

Alcoholism Clin & Exp Res

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“…The immune system is one candidate mediator of the alcohol hangover. Studies have shown inflammatory effects after acute alcohol administration, such as significantly elevated serum cytokine levels 2 h after drinking [ 7 ]. It has been hypothesized that these inflammatory effects persist over longer time, and/or have an influence on the presence or severity of a next-day alcohol hangover [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Susceptibility to Alcohol Hangovers: The Association with Self-Reported Immune Status

Loo

Mackus

Lantman

et al. 2018

IJERPH

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Increasing evidence points at a role for the immune system in the genesis of the alcohol hangover. This study investigated the association between self-reported immune function and experiencing hangovers. Dutch students aged 18 to 30 years old were invited to complete an online survey. Eighteen items on immune-related complaints were completed to assess self-reported immune function. Alcohol consumption in the past month (with respect to usual consumption and the occasion of heaviest drinking) was also recorded. Subjects with an estimated blood alcohol concentration (eBAC) of 0.18% or higher on their heaviest drinking occasion in the prior month were included in the analyses. Self-reported immune function was compared between drinkers with a hangover and those who claimed to be hangover resistant. In total, of 481 subjects (79.2% women) with a mean (SD) age of 21.1 (1.9) years old were included in the analysis. Of these, 83.3% (n = 400) reported having hangovers and 16.8% (n = 81) claimed to be hangover resistant. Drinkers with hangovers had significantly higher self-reported overall immune function scores when compared to hangover-resistant drinkers (mean ± SD = 10.5 ± 3.6 versus 13.1 ± 4.9, p = 0.0001), indicating a poorer immune status. In conclusion, experiencing alcohol hangovers is associated with significantly poorer self-reported immune function.

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“…Although a blood alcohol concentration (BAC) of 0.08% (17.4 mM) is the legal limit for driving in the United States and many other countries, much higher BACs can be reached following acute heavy alcohol consumption [49, 50]. As such, a BAC of 0.4% (87 mM) is typically lethal in humans.…”

Section: Discussionmentioning

confidence: 99%

p53 pathway determines the cellular response to alcohol-induced DNA damage in MCF-7 breast cancer cells

et al. 2017

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Alcohol consumption is associated with increased breast cancer risk; however, the underlying mechanisms that contribute to mammary tumor initiation and progression are unclear. Alcohol is known to induce oxidative stress and DNA damage; likewise, p53 is a critical modulator of the DNA repair pathway and ensures genomic integrity. p53 mutations are frequently detected in breast and other tumors. The impact of alcohol on p53 is recognized, yet the role of p53 in alcohol-induced mammary carcinogenesis remains poorly defined. In our study, we measured alcohol-mediated oxidative DNA damage in MCF-7 cells using 8-OHdG and p-H2AX foci formation assays. p53 activity and target gene expression after alcohol exposure were determined using p53 luciferase reporter assay, qPCR, and Western blotting. A mechanistic study delineating the role of p53 in DNA damage response and cell cycle arrest was based on isogenic MCF-7 cells stably transfected with control (MCF-7/Con) or p53-targeting siRNA (MCF-7/sip53), and MCF-7 cells that were pretreated with Nutlin-3 (Mdm2 inhibitor) to stabilize p53. Alcohol treatment resulted in significant DNA damage in MCF-7 cells, as indicated by increased levels of 8-OHdG and p-H2AX foci number. A p53-dependent signaling cascade was stimulated by alcohol-induced DNA damage. Moderate to high concentrations of alcohol (0.1–0.8% v/v) induced p53 activation, as indicated by increased p53 phosphorylation, reporter gene activity, and p21/Bax gene expression, which led to G0/G1 cell cycle arrest. Importantly, compared to MCF-7/Con cells, alcohol-induced DNA damage was significantly enhanced, while alcohol-induced p21/Bax expression and cell cycle arrest were attenuated in MCF-7/sip53 cells. In contrast, inhibition of p53 degradation via Nutlin-3 reinforced G0/G1 cell cycle arrest in MCF-7 control cells. Our study suggests that functional p53 plays a critical role in cellular responses to alcohol-induced DNA damage, which protects the cells from DNA damage associated with breast cancer risk.

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Cytokine Changes following Acute Ethanol Intoxication in Healthy Men: A Crossover Study

Cited by 40 publications

References 28 publications

Time Course of Blood and Brain Cytokine/Chemokine Levels Following Adolescent Alcohol Exposure and Withdrawal in Rats

Time Course of Blood and Brain Cytokine/Chemokine Levels Following Adolescent Alcohol Exposure and Withdrawal in Rats

Susceptibility to Alcohol Hangovers: The Association with Self-Reported Immune Status

p53 pathway determines the cellular response to alcohol-induced DNA damage in MCF-7 breast cancer cells

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