Drinking pattern and socio-cultural aspects on immune response: an overview

Romeo, Javier; Wärnberǵ, Julia; Marcos, Ascensión

doi:10.1017/s0029665110001904

Cited by 22 publications

(14 citation statements)

References 70 publications

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“…First of all, our study is limited to the comparison of only two most common utilized durations of chronic alcohol exposure of 4 weeks for LD diet and 12 weeks of MC model so two different magnitudes of alcohol exposure 22,[24][25][26][27][28][29] . However, it is pretty well known that alcohol effects on specific immune cells and tissue injury are highly dependent of alcohol exposure time [56][57][58][59] . For example, alcohol decreases NK cell proliferation at 2 weeks while increases splenic NK cell pool at 3 months 19 .…”

Section: Discussionmentioning

confidence: 99%

Restricted immunological and cellular pathways are shared by murine models of chronic alcohol consumption

Vogle

Qian

Zhu

et al. 2020

Sci Rep

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Murine models of chronic alcohol consumption are frequently used to investigate alcoholic liver injury and define new therapeutic targets. Lieber-DeCarli diet (LD) and Meadows-Cook diet (MC) are the most accepted models of chronic alcohol consumption. It is unclear how similar these models are at the cellular, immunologic, and transcriptome levels. We investigated the common and specific pathways of LD and MC models. Livers from LD and MC mice were subjected to histologic changes, hepatic leukocyte population, hepatic transcripts level related to leukocyte recruitment, and hepatic RNA-seq analysis. Cross-species comparison was performed using the alcoholic liver disease (ALD) transcriptomic public dataset. Despite LD mice have increased liver injury and steatosis by alcohol exposure, the number of CD45 + cells were reduced. Opposite, MC mice have an increased number of monocytes/liver by alcohol. The pattern of chemokine gradient, adhesion molecules, and cytokine transcripts is highly specific for each model, not shared with advanced human alcoholic liver disease. Moreover, hepatic RNA-seq revealed a limited and restricted number of shared genes differentially changed by alcohol exposure in these 2 models. Thus, mechanisms involved in alcohol tissue injury are model-dependent at multiple levels and raise the consideration of significant pathophysiological diversity of human alcoholic liver injury. Murine models are frequently used to investigate new pathophysiological pathways of human diseases and many new treatment trials for alcoholic liver disease (ALD) are based on preclinical testing provided by murine models. ALD in humans is the result of a complex interaction between the alcoholic effects on gut microbiota, intestinal cells, immune system, and the hepatic microenvironment 1,2. Based on an extensive body of literature, alcohol increases the intestinal permeability and subsequent systemic translocation of bacterial products, e.g. LPS 1,3,4. Stimulation of Toll-like receptors (TLR) by bacterial products results in immune cell activation related to hepatic alcohol metabolic process that has a deleterious effect on the liver, resulting in histological features of ALD: steatosis, innate immune infiltrate with predominance of neutrophils and monocytes, and histological signs of hepatocyte dysfunction (Mallory hyaline formation, ballooning hepatocyte) 3,5-7. ALD includes a spectrum of histological and clinical entities: steatosis, steatohepatitis, and alcoholic hepatitis 8,9. In time, chronic liver injury with a dysregulated innate immune response results in alcohol-induced progressive hepatic fibrogenesis, liver cirrhosis and end-stage liver disease 10. Based on this classical paradigm, few trials have been attempted to control an exacerbated innate immune response or to improve hepatocyte function. Besides steroids that may be beneficial for only subsets of patients with alcoholic hepatitis 11 , no other treatments have proven consistent survival benefit 12. Moreover, treatment of anti-TNFα in alcoholic hepati...

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Section: Discussionmentioning

confidence: 99%

Restricted immunological and cellular pathways are shared by murine models of chronic alcohol consumption

Vogle

Qian

Zhu

et al. 2020

Sci Rep

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“…Although alcohol consumption has been reported to impair the development of both innate and adaptive immune responses [ 1 ], the effects of alcohol on the innate immune system are controversial. Overall, alcohol has been known to be an immune-modulator with high alcohol consumption reported to induce inflammation while moderate alcohol consumption reported to possibly have a beneficial impact on the immune system [ 2 – 4 ]. Dendritic cells (DCs) play a crucial role during inflammation and have been shown to be affected during alcohol abuse.…”

Section: Introductionmentioning

confidence: 99%

Profile of Class I Histone Deacetylases (HDAC) by Human Dendritic Cells after Alcohol Consumption and In Vitro Alcohol Treatment and Their Implication in Oxidative Stress: Role of HDAC Inhibitors Trichostatin A and Mocetinostat

et al. 2016

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Epigenetic mechanisms have been shown to play a role in alcohol use disorders (AUDs) and may prove to be valuable therapeutic targets. However, the involvement of histone deacetylases (HDACs) on alcohol-induced oxidative stress of human primary monocyte-derived dendritic cells (MDDCs) has not been elucidated. In the current study, we took a novel approach combining ex vivo, in vitro and in silico analyses to elucidate the mechanisms of alcohol-induced oxidative stress and role of HDACs in the periphery. ex vivo and in vitro analyses of alcohol-modulation of class I HDACs and activity by MDDCs from self-reported alcohol users and non-alcohol users was performed. Additionally, MDDCs treated with alcohol were assessed using qRT-PCR, western blot, and fluorometric assay. The functional effects of alcohol-induce oxidative stress were measured in vitro using PCR array and in silico using gene expression network analysis. Our findings show, for the first time, that MDDCs from self-reported alcohol users have higher levels of class I HDACs compare to controls and alcohol treatment in vitro differentially modulates HDACs expression. Further, HDAC inhibitors (HDACi) blocked alcohol-induction of class I HDACs and modulated alcohol-induced oxidative stress related genes expressed by MDDCs. In silico analysis revealed new target genes and pathways on the mode of action of alcohol and HDACi. Findings elucidating the ability of alcohol to modulate class I HDACs may be useful for the treatment of alcohol-induced oxidative damage and may delineate new potential immune-modulatory mechanisms.

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“…It is tempting to speculate that higher chronic alcohol use could have led to decreased immune function, whereas acute alcohol use over SB may have had a stimulating effect on immune function. However, the relationship between alcohol exposure and health is multifactorial and contingent on issues such as the amount and variability of drinking over time, as well as the type of alcohol consumed [45] . Binary logistic regression analyses did not reveal any significant associations between drinking and IgA:albumin as predictors of cortisol response group.…”

Section: Discussionmentioning

confidence: 99%

Stress, Immune Function and Collegiate Holiday Drinking: A Pilot Study

Ceballos

Sharma²,

Patterson³

et al. 2015

Neuropsychobiology

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Background/Aims: Social aspects of collegiate holiday drinking have been studied frequently, but physiological consequences are often overlooked. This study examined self-reported stress, endocrine and immune indicators in students at an American university before and after their week-long spring break (SB) holiday. Methods: Participants (n = 27; 9 males) provided saliva samples and completed surveys pre- and post-SB. Based on their cortisol reaction to SB, participants were grouped as cortisol nonresponders (CNR; n = 14) or increasers (CI; n = 13). Groups were matched on demographics, baseline alcohol use, family history of alcoholism, and SB plans. Differences over time and between groups were examined for α-amylase, quantity/frequency of alcohol use (quantity/frequency index, QFI) and the immunoglobulin A (IgA) to albumin ratio (IgA:albumin). Results: α-Amylase decreased over time. A time × group interaction was noted for QFI, in which CNRs increased drinking over SB, but CIs did not. Time and time × group effects occurred for IgA:albumin. CIs decreased IgA:albumin over SB, whereas CNRs did not. Pre-SB QFI and pre-/post-SB QFI changes were correlated with changes in IgA:albumin. Conclusion: These findings support previously published relationships between blunted cortisol responses and risk for problem drinking, as well as elevated cortisol and decreased immune response. These data also highlight the importance of physiological measures in the study of collegiate holiday drinking.

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Drinking pattern and socio-cultural aspects on immune response: an overview

Cited by 22 publications

References 70 publications

Restricted immunological and cellular pathways are shared by murine models of chronic alcohol consumption

Restricted immunological and cellular pathways are shared by murine models of chronic alcohol consumption

Profile of Class I Histone Deacetylases (HDAC) by Human Dendritic Cells after Alcohol Consumption and In Vitro Alcohol Treatment and Their Implication in Oxidative Stress: Role of HDAC Inhibitors Trichostatin A and Mocetinostat

Stress, Immune Function and Collegiate Holiday Drinking: A Pilot Study

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