Disturbance of Human Immunohomeostasis by Environmental Pollution and Alcohol Consumption

Kazbarienė, Birutė; Krikstaponiene, Aurelija; Moncevičiūtė-Eringienė, Elena

doi:10.1556/amicr.53.2006.2.7

Cited by 6 publications

(6 citation statements)

References 10 publications

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“…Moreover, elevated LPS and sCD14 are induced by acute alcohol exposure and are reported in early alcohol withdrawal (Bala, Marcos, Gattu, Catalano, & Szabo, 2014; Frank, Witte, Schrodl, & Schutt, 2004; Leclercq et al, 2012). In a community sample, consuming ≥5 drinks one or more times per week was associated with lower EndoCAb (Kazbariene, Krikstaponiene, & Monceviciute-Eringiene, 2006). …”

Section: Introductionmentioning

confidence: 99%

Alcohol use predicts elevation in inflammatory marker soluble CD14 in men living with HIV

et al. 2016

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Independently, HIV infection and heavy alcohol use increase microbial translocation of gut products into systemic circulation. Microbial translocation and consequent immune response have been linked to chronic inflammation and a host of negative health outcomes in individuals living with HIV. However, previous research has not systematically investigated the immune correlates of heavy drinking specifically within the HIV-positive population. This pilot study investigated microbial translocation and immune activation as a function of alcohol use in 21 HIV-positive men who met NIAAA criteria for heavy drinking. Participants averaged 46.7 ± 8.5 (mean ± standard deviation) years of age, 12.2 ± 9.2 years since HIV diagnosis, 337 ± 158 CD4 nadir, and 643 ± 245 current CD4 count. All participants were virologically suppressed on antiretroviral therapy. Data on alcohol use and immune function were collected at baseline and three-month follow-up. Plasma concentrations of markers of microbial translocation and immune activation [lipopolysaccharide (LPS), soluble CD14 (sCD14), endotoxin core antibody immunoglobulin M (EndoCAb)] were measured using enzyme-linked immunosorbent assays. Generalized estimating equation models tested alcohol use variables as predictors of LPS, sCD14, and EndoCAb levels. Greater quantity and frequency of drinking significantly predicted higher sCD14 levels (p’s <.01). Conversely, longer duration of abstinence from alcohol significantly predicted lower sCD14 levels (p <.001). These results remained significant after controlling for age, HIV duration, smoking status, current CD4 count, CD4 nadir, and antiretroviral drug type. In addition, participants with ≥50% relative reduction in drinks per week showed a significant decrease (p <.05) in sCD14 from baseline to three-month follow-up. This pilot study provides preliminary evidence that heavy drinking may increase a key inflammatory marker in HIV-infected individuals with suppressed infection.

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Section: Introductionmentioning

confidence: 99%

Alcohol use predicts elevation in inflammatory marker soluble CD14 in men living with HIV

et al. 2016

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“…In human studies, alcoholic patients have significantly reduced numbers of CD4 + T lymphocytes and recovery of the CD4 + T lymphocyte count has been noted in several studies after alcohol withdrawal, suggesting that ethanol can directly affect CD4 + T lymphocyte survival (13)(14)(15)(16)(17)(18). CD4 + T lymphocytes are the central regulators of the immune system, controlling both cell-mediated and humoral immunity.…”

Section: Introductionmentioning

confidence: 99%

Ethanol inhibits methionine adenosyltransferase II activity and S-adenosylmethionine biosynthesis and enhances caspase-3-dependent cell death in T lymphocytes: relevance to alcohol-induced immunosuppression

Hote¹,

Sahoo²,

Jani³

et al. 2008

The Journal of Nutritional Biochemistry

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An important aspect in alcohol abuse associated immune suppression is the loss of T helper CD4 + lymphocytes leading to an impairment of multiple immune functions. Our work has shown that ethanol can sensitize CD4 + T lymphocytes to activation-induced, caspase-3 dependent cell death (AICD). It has been demonstrated that formation of S-adenosylmethionine (SAMe) catalyzed by methionine adenosyltransferase II (MAT II) is essential for CD4 + T cell activation and proliferation. Since ethanol is known to affect SAMe metabolism in hepatocytes, we investigated the effect of ethanol on MAT II activity/expression, SAMe biosynthesis and cell survival in CD4 + T lymphocytes. We demonstrate for the first time that ethanol at a physiologically relevant concentration (25mM) substantially decreased the enzymatic activity of MAT II in T lymphocytes. Ethanol was observed to decrease the transcription of MAT2A, which encodes the catalytic subunit of MAT II and is vital for MAT II activity and SAMe biosynthesis. Further, correspondent to its effect on MAT II, ethanol decreased intracellular SAMe levels and enhanced caspase-3 dependent AICD. Importantly, restoration of intracellular SAMe levels by exogenous SAMe supplementation considerably decreased both caspase-3 activity and apoptotic death in T lymphocytes. In conclusion, our data shows that MAT II and SAMe are critical molecular components essential for CD4 + T cell survival which are affected by ethanol leading to enhanced Address correspondence to: Shirish Barve PhD, Professor, Department of Medicine, Pharmacology and Toxicology, University of Louisville Medical Center, 511 S. Floyd, MDR Bldg., Rm#526, Louisville, KY 40202. Tel. 502 852 -5245; Fax. 502 562 -4271; shirish.barve@louisville.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AICD. Furthermore, these studies provide a clinical paradigm for the development of the much needed therapy using SAMe supplementation in the treatment of immune dysfunction induced by alcohol abuse. HHS Public Access

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“…In addition, the course of infection in alcoholics is more severe and often associated with increased morbidity and mortality (3, 4). Alcohol dependent patients displayed a decrease in peripheral CD4+ve T cells, which recovered after alcohol with drawl (5–10). Chronic ethanol administration in animals also resulted in reduction of both peripheral and splenic CD4 +ve T cells (11–18).…”

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confidence: 99%

Ethanol and Vitamin D Receptor in T Cell Apoptosis

Rehman

Chandel

Salhan

et al. 2012

J Neuroimmune Pharmacol

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Ethanol has been demonstrated to cause T cell apoptosis. In the present study, we evaluated the role of VDR and the renin angiotensin system (RAS) in oxidative stress-induced T cell apoptosis. Ethanol-treated human T cells displayed down regulation of vitamin D receptor (VDR) and the activation of the RAS in the form of enhanced T cell renin expression and angiotensin II (Ang II) production. The silencing of VDR with siRNA displayed the activation of the RAS, and activation of the VDR resulted in the down regulation of the RAS. It suggested that ethanol-induced T cell RAS activation was dependent on the VDR status. T cell ROS generation by ethanol was found to be dose dependent. Conversely, ethanol-induced ROS generation was inhibited if VDR was activated or Ang II was blocked by an angiotensin II type 1 (AT1) receptor blocker (Losartan). Furthermore, it was observed that ethanol not only induced double strand breaks in T cells but also attenuated DNA repair response, whereas, VDR activation inhibited ethanol-induced double strand breaks and also enhanced DNA repairs. Since free radical scavengers inhibited ethanol-induced DNA damage, it would indicate that ethanol-induced DNA damage was mediated through ROS generation. These findings indicated that ethanol-induced T cell apoptosis was mediated through ROS generation in response to ethanol-induced down regulation of VDR and associated activation of the RAS.

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Disturbance of Human Immunohomeostasis by Environmental Pollution and Alcohol Consumption

Cited by 6 publications

References 10 publications

Alcohol use predicts elevation in inflammatory marker soluble CD14 in men living with HIV

Alcohol use predicts elevation in inflammatory marker soluble CD14 in men living with HIV

Ethanol inhibits methionine adenosyltransferase II activity and S-adenosylmethionine biosynthesis and enhances caspase-3-dependent cell death in T lymphocytes: relevance to alcohol-induced immunosuppression

Ethanol and Vitamin D Receptor in T Cell Apoptosis

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