Metabolic Consequences of Alcohol Ingestion

Preedy, Victor R.

doi:10.1002/9780470515549.ch3

Cited by 15 publications

(8 citation statements)

References 29 publications

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“…Studies have shown decreases in the production of TNF-α, IL-1β, and IL-6 by cells, including, but not limited to, neutrophils and macrophages, after in vivo or in vitro ethanol exposure (Nelson and others 1989b;Verma and others 1993;Szabo and others 1996;Szabo 1998;Boe and others 2001;Goral and others 2004;Goral and Kovacs 2005). Some attribute these effects to alterations in the integrity of cellular membranes, specifically due to increased fluidity (Peters and Preedy 1998). Membrane alteration can influence lipid raft stability, which are known to be involved in cell signaling (Simons and Toomre 2000;Pike 2003).…”

Section: Discussionmentioning

confidence: 99%

Acute Ethanol Exposure Attenuates Pattern Recognition Receptor Activated Macrophage Functions

Karavitis

Murdoch²,

Gómez³

et al. 2008

Journal of Interferon & Cytokine Research

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Both clinical and experimental data have linked acute ethanol exposure to increased susceptibility to infection as well as increased morbidity and mortality after injury. Macrophages play an integral role in the innate immune system and are important in priming the adaptive immune system. In this study, we investigated the effect of a single in vivo exposure of macrophages to physiologically relevant levels of ethanol (1.2 and 2.9 g/kg) followed by ex vivo stimulation with lipopolysaccharide (LPS) or bacteria. Our study confirms the work of others showing that a single administration of ethanol suppresses the production of tumor necrosis factor-alpha(TNF-alpha), interleukin-6 (IL-6), and IL-12 in response to LPS. There was no effect of ethanol on LPS induction of cytokine production at 30 min after treatment. In contrast, at 3 h, both doses of ethanol exposure decreased ex vivo TNF-alpha production by splenic and alveolar macrophages. Interestingly, the higher dose of ethanol resulted in sustained suppression of LPS-induced TNF-alpha production at 3 and 6 h after ethanol administration, as well as decreased IL-6 and IL-12 production after 6 h, as compared to control (saline-treated groups). Alveolar macrophages behaved similarly at 3 h after ethanol treatment. LPS-stimulated production of TNF-alpha and IL-6 was reduced at 3 h after ethanol administration, when compared with the saline-treated animals. Alveolar macrophages stimulated for 3 h with bacteria also showed decreased TNF-alpha and IL-6 production after harvested from mice given 2.9 g/kg ethanol for 3 h. This time point and high dose of ethanol also resulted in decreased Pseudomonas aeruginosa phagocytosis by alveolar macrophages. Taken together, we conclude that the effects of physiological levels of ethanol are dose dependent, have effects that last after ethanol is cleared from the circulation, and can affect multiple macrophage functions.

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Section: Discussionmentioning

confidence: 99%

Acute Ethanol Exposure Attenuates Pattern Recognition Receptor Activated Macrophage Functions

Karavitis

Murdoch²,

Gómez³

et al. 2008

Journal of Interferon & Cytokine Research

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“…Ethanol interacts with membrane lipids and influences the function of membrane proteins (138). Acute ethanol treatment is known to increase membrane fluidity (139), which may interfere with receptor clustering and signal transduction processes. Conversely, the fluidizing effects of ethanol during chronic ethanol exposure are counterbalanced by changes in membrane lipids toward more saturated fatty acids (140), allowing TLRs specific ligands binding and exacerbating the inflammatory response.…”

Section: Ethanol and Innate Immune Systemmentioning

confidence: 99%

Ethanol intake enhances inflammatory mediators in brain: role of glial cells and TLR4/IL-1RI receptors

Blanco

Guerri²

2007

Front Biosci

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The brain is one of the major target organs of ethanol actions, and its chronic and acute intoxication results in significant alterations in brain structure and function, and in some cases to neurodegeneration. Glial cells and Toll-like receptors (TLRs) are vital players in CNS immune response; dysregulation of this response plays an important role in brain damage and neurodegeneration. Ethanol has immunomodulatory effects and induces specific alterations in the TLRs response in many tissues. These actions depend on the cell type, ethanol dose and treatment duration, as well as the concomitant presence of pathogens and their characteristics. Recent findings indicate that low concentrations of ethanol (10 mM) promote inflammatory processes in brain and in glial cells by up-regulating cytokines and inflammatory mediators (iNOS, NO, COX-2), and by activating signaling pathways (IKK, MAPKs) and transcriptional factors (NF-kappaB, AP-1) implicated in inflammatory injury. TLR4/IL-1RI receptors may be involved in ethanol-mediated inflammatory signaling, since blocking these receptors abolishes the production of ethanol-induced inflammatory mediators and cell death. We propose that at low physiologically relevant concentrations, ethanol facilitates TLR4/IL-1RI recruitment into lipid rafts microdomains, leading to the activation and signaling of these receptors. In summary, current results suggest that TLR4/ IL-1RI are important targets of ethanol-induced inflammatory brain damage.

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“…Moreover, we also reported that physiologically relevant levels of EtOH induced the mRNA expression of hypoxia‐inducible factor 1 α (HIF‐1α) in cultured vascular smooth muscle cells 19. The classic pathway for EtOH metabolism is oxidation of EtOH to form acetaldehyde, a process that is catalyzed by alcohol dehydrogenase 30. An important consequence of EtOH and acetaldehyde oxidation is an increase in both cytosolic and mitochondrial reduced nicotinamide adenine dinucleotide/nicotinamide adenine dinucleotide (NADH/NAD).…”

Section: Discussionmentioning

confidence: 99%

Ethanol stimulates tumor progression and expression of vascular endothelial growth factor in chick embryos

Bailey

Sartin

et al. 2005

Cancer

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BACKGROUND The mechanisms by which alcohol consumption causes cancer have not been established due to a lack of experimental studies. METHODS A chick embryo chorioallantoic membrane (CAM) model that bore human fibrosarcoma (HT1080) was used to determine whether the administration of physiologically relevant doses of ethanol could stimulate tumor growth, angiogenesis, metastasis, and vascular endothelial growth factor (VEGF) expression in tumors. HT1080 cells were inoculated onto the “upper CAM” on Day 8, saline or ethanol was administrated at a dose of 0.25g/kg per day on the CAM, and the tumors were harvested on Day 17. VEGF mRNA and protein were determined by Northern blot analysis and enzyme‐linked immunosorbent assay. Intratumoral vascular volume density (IVVD) was determined by point counting on periodic acid–Schiff‐stained sections. Intravasation of HT1080 cells was determined using human‐Alu polymerase chain reaction analysis. The effects of ethanol on VEGF expression and cell proliferation were examined in cultured HT1080 cells. RESULTS Ethanol treatment for 9 days caused a 2.2‐fold increase in tumor volume (867 ± 138 mm3 vs. 402 ± 28 mm3), a 2.1‐fold increase in IVVD (0.021 ± 0.004 mm3/mm3 vs. 0.010 mm3/mm3 ± 0.002 mm3/mm3), and a significant increase in VEGF mRNA or protein expression in tumors compared with a group of control embryos (n = 6 embryos; P < 0.01). Ethanol treatment caused an increase > 8‐fold in the intravasated HT1080 cells in the CAM group compared with the control group (n = 6 embryos; P < 0.01). Physiologically relevant levels of ethanol (10 mM and 20 mM) caused a dose‐related increase in VEGF mRNA and protein expression in cultured HT1080 cells. The ethanol–HT1080‐conditioned media increased the proliferation of endothelial cells, but not of HT1080 cells. CONCLUSIONS The findings suggest that the induction of angiogenesis and VEGF expression by ethanol represents an important mechanism of cancer progression associated with alcoholic beverage consumption. Cancer 2005. © 2004 American Cancer Society.

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Metabolic Consequences of Alcohol Ingestion

Cited by 15 publications

References 29 publications

Acute Ethanol Exposure Attenuates Pattern Recognition Receptor Activated Macrophage Functions

Acute Ethanol Exposure Attenuates Pattern Recognition Receptor Activated Macrophage Functions

Ethanol intake enhances inflammatory mediators in brain: role of glial cells and TLR4/IL-1RI receptors

Ethanol stimulates tumor progression and expression of vascular endothelial growth factor in chick embryos

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