Alcohol and inflammation and immune responses: summary of the 2006 Alcohol and Immunology Research Interest Group (AIRIG) meeting

Waldschmidt, Thomas J.; Cook, Robert T.; Kovacs, Elizabeth J.

doi:10.1016/j.alcohol.2007.11.003

Cited by 45 publications

(41 citation statements)

References 35 publications

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“…It is known that alcoholics are more susceptible to infections. 4,6 Because streptococcal infections are trigger factors for psoriasis, 7 this increased susceptibility may be involved in the onset and progress of the disease.…”

Section: Alcohol Alters the Immune Systemmentioning

confidence: 99%

Psoriasis and alcohol: is cutaneous ethanol one of the missing links?

Farkas

Kemény

2009

British Journal of Dermatology

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Many exogenous factors including excessive alcohol consumption have been associated with psoriasis, but the underlying mechanisms still remain elusive. Drinking worsens therapeutic compliance, and decreases the efficacy and increases the toxicity of systemic antipsoriatic treatments. Excess alcohol intake results in compromised immunity and increased risk of infections, but alcohol can induce proinflammatory cytokine production in various cell types and can increase mitogen-derived lymphocyte proliferation and lymphocyte activation. As we have previously reported, alcohol and one of its metabolites, acetone, induce keratinocyte proliferation and increase the mRNA levels of genes characteristic for proliferating keratinocytes, such as alpha5 integrin, cyclin D1 and keratinocyte growth factor receptor. Recently the correlation between blood and skin ethanol levels in humans was determined by a transdermal alcohol monitoring device, against the 'gold standard' breath alcohol readings. Based on transdermal alcohol measurements it can be concluded that cutaneous alcohol concentrations can reach levels that induce proinflammatory cytokine production and lymphocyte and keratinocyte proliferation in vitro. It is expected that the development of methodologies measuring transdermal ethanol will provide additional tools to evaluate how alcohol influences skin physiology and different dermatological conditions including psoriasis. Our review focuses on the possible link between alcohol misuse and psoriasis, particularly on the possible role of cutaneous ethanol in precipitating the disease.

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Section: Alcohol Alters the Immune Systemmentioning

confidence: 99%

Psoriasis and alcohol: is cutaneous ethanol one of the missing links?

Farkas

Kemény

2009

British Journal of Dermatology

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“…ethanol and antioxidants) that potentially counteract systemic inflammation, decreasing cellular responses to immunogens, and suppressing synthesis of pro-inflammatory cytokines, such as tumor necrosis factor (TNF), interleukin (IL)-6, IL-8, both in vivo and in vitro in alveolar macrophages and human blood monocytes [84]. Antioxidants in wine and beer influence cytokines such as interferon-gamma in vitro and may inhibit key enzymes involved in DNA synthesis [85,86].…”

Section: Occupational Exposures and Environmental Pollutantsmentioning

confidence: 99%

Understanding the role of environmental factors in the development of systemic lupus erythematosus

Parks

Santos

Barbhaiya

et al. 2017

Best Practice & Research Clinical Rheumatology

169

121

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Systemic lupus erythematosus (SLE) is a multisystem disease with a complex etiology. Risk is higher among women, racial and ethnic minorities, and individuals with a family history of SLE or related autoimmune diseases. It is thought that genetic factors interact with environmental exposures throughout the lifespan to influence susceptibility to developing SLE. The strongest epidemiologic evidence exists for increased risk of SLE associated with exposure to crystalline silica, current cigarette smoking, use of oral contraceptives and postmenopausal hormone replacement therapy, while there is an inverse association with alcohol use. Emerging research results suggest possible associations of SLE risk with exposure to solvents, residential and agricultural pesticides, heavy metals, and air pollution. Ultraviolet light, certain infections, and vaccinations have also been hypothesized to be related to SLE risk. Mechanisms linking environmental exposures and SLE include epigenetic modifications resulting from exposures, and increased oxidative stress, systemic inflammation and inflammatory cytokine upregulation, and hormonal effects. Research needs to include new studies of environmental risk factors for SLE generally, with a focus on lifetime exposure assessment, and studies in susceptible subgroups, such as family members or based on genetic risk profiles, or in individuals with evidence of pre-clinical autoimmunity based on detection of specific auto-antibodies. Understanding the role of environmental exposures in the development of SLE may help to identify modifiable risk factors and potential etiologic mechanisms.

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“…For example, fermented alcohols, especially wines, are suggested to have polyphenols that can reduce inflammation [12, 13]. Alcoholic beverages that are made through distillation (i.e., “purification”) processes, such as liquor, might be deficient of such “beneficial” chemicals, and the ethanol in such drinks could in turn be more inflammatory [14]. Alternatively, imperfectly processed “locally-made” drinks may retain excessive levels of harmful non-ethanol chemicals like methanol [15], which could promote inflammation.…”

Section: Introductionmentioning

confidence: 99%

Alcohol Types and HIV Disease Progression Among HIV-Infected Drinkers Not Yet on Antiretroviral Therapy in Russia and Uganda

et al. 2017

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Objectives In HIV-infected drinkers, alcohol types more likely to cause inflammation could plausibly increase the risk of HIV disease progression. We therefore assessed the association between alcohol type and plasma HIV RNA level (HIV viral load) among HIV-infected drinkers not on antiretroviral therapy (ART) in Russia and Uganda. Methods We analyzed the data of participants from cohorts in Russia and Uganda and assessed their HIV viral load at enrollment by the alcohol type predominantly consumed. We defined predominant alcohol type as the alcohol type contributing >50% of total alcohol consumption in the 1 month (Russia) or 3 months (Uganda) prior to enrollment. Using multiple linear regression, we compared log10 HIV viral load by predominant alcohol type, controlling for age, gender, socioeconomic status, total number of standard drinks, frequency of drinking ≥6 drinks/occasion, and in Russia, history of injection drug use. Results Most participants (99.2% of 261 in Russia and 98.9% of 352 in Uganda) predominantly drank one alcohol type. In Russia, we did not find evidence for differences in viral load levels between drinkers of fortified wine (n=5) or hard liquor (n=49), compared to drinkers of beer/low-ethanol-content cocktails (n=163); however, wine/high-ethanol-content cocktail drinkers (n=42) had higher mean log10 viral load than beer/low-ethanol-content cocktail drinkers (β=0.38, 95%CI: 0.07 to 0.69; p=0.02). In Uganda, we did not find evidence for differences in viral load levels between drinkers of locally-brewed beer (n=41), commercially-distilled spirits (n=38), or locally-distilled spirits (n=43), compared to drinkers of commercially-made beer (n=218); however, wine drinkers (n=8) had lower mean log10 HIV viral load (β=−0.65, 95% CI −1.36 to 0.07, p = 0.08), although this did not reach statistical significance. Conclusions Among HIV-infected drinkers not yet on ART in Russia and Uganda, we observed an association between the alcohol type predominantly consumed and the HIV viral load level in the Russia sample. These exploratory results suggest that, in addition to total number of drinks and drinking patterns, alcohol type might be a dimension of alcohol use that merits examination in studies of HIV and alcohol related outcomes.

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Alcohol and inflammation and immune responses: summary of the 2006 Alcohol and Immunology Research Interest Group (AIRIG) meeting

Cited by 45 publications

References 35 publications

Psoriasis and alcohol: is cutaneous ethanol one of the missing links?

Psoriasis and alcohol: is cutaneous ethanol one of the missing links?

Understanding the role of environmental factors in the development of systemic lupus erythematosus

Alcohol Types and HIV Disease Progression Among HIV-Infected Drinkers Not Yet on Antiretroviral Therapy in Russia and Uganda

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