Alcohol takes the toll on immune function

Stadlbauer, Vanessa; Shah, Naina; Arjona, M. Montes de Oca; Mookerjee, Rajeshwar P.; Jalan, Rajiv

doi:10.1111/j.1478-3231.2010.02271.x

Cited by 3 publications

(1 citation statement)

References 19 publications

(24 reference statements)

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“…The detrimental effects of ethanol on health are numerous, and its most important side effect is damage to the liver ( 1 , 2 ). Ethanol consumption initiates immune response that may lead to liver damage and consequently, alcoholic liver disease (ALD) ( 3 , 4 ). In the course of ALD, the infiltration of immune cells like neutrophils, macrophages, T cells, and B cells further induces pro-inflammatory cytokines and chemokine, resulting in hepatic inflammation and tissue damage ( 5 – 8 ).…”

Section: Introductionmentioning

confidence: 99%

Expansion of Granulocytic, Myeloid-Derived Suppressor Cells in Response to Ethanol-Induced Acute Liver Damage

Wang

Tan

et al. 2018

Front. Immunol.

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The dual role of ethanol in regulating both pro-inflammatory and anti-inflammatory response has recently been reported. Myeloid-derived suppressor cells (MDSCs) are one of the major components in the immune suppressive network in both innate and adaptive immune responses. In this study, we aim to define the role of a population expressing CD11b+Ly6GhighLy6Cint with immunosuppressive function in response to ethanol-induced acute liver damage. We find this increased granulocytic-MDSCs (G-MDSCs) population in the blood, spleen, and liver of mice treated with ethanol. Depletion of these cells increases serum alanine aminotransferase and aspartate aminotransferase levels, while G-MDSCs population adoptive transfer can ameliorate liver damage induced by ethanol, indicating the protective role in the early stage of alcoholic liver disease. The significant changes of T-cell profiles after G-MDSCs populations adoptive transfer and anti-Gr1 injection signify that both cytotoxic T and T helper cells might be the targeted cells of G-MDSCs. In the in vitro study, we find that myeloid precursors preferentially generate G-MDSCs and improve their suppressive capacity via chemokine interaction and YAP signaling when exposed to ethanol. Furthermore, IL-6 serves as an important indirect factor in mediating the expansion of G-MDSCs populations after acute ethanol exposure. Collectively, we show that expansion of G-MDSCs in response to ethanol consumption plays a protective role in acute alcoholic liver damage. Our study provides novel evidence of the immune response to acute ethanol consumption.

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Section: Introductionmentioning

confidence: 99%

Expansion of Granulocytic, Myeloid-Derived Suppressor Cells in Response to Ethanol-Induced Acute Liver Damage

Wang

Tan

et al. 2018

Front. Immunol.

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Bench-to-beside review: Acute-on-chronic liver failure - linking the gut, liver and systemic circulation

2011

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The concept of acute-on-chronic liver failure (ACLF) was introduced recently to describe a subset of patients with chronic liver disease presenting with profound deterioration of liver function and rapidly evolving multi-organ failure. ACLF is frequently accompanied by the development of severe inflammatory response syndrome and has a high mortality. To date, treatment options are limited and exclusively supportive. Over the last few years, some insights have been generated in the pathophysiology of ACLF. A key role for the interaction of innate immune dysfunction, enhanced bacterial translocation from the gut, and circulatory dysfunction has been proposed. In this respect, therapeutic strategies have been examined, with variable success, in experimental studies in animals and humans. This review focuses on potentially relevant pathophysiological elements in the development of ACLF and points out promising treatment modalities in ACLF.

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Blood culture-positive infections in patients with alcoholic hepatitis

Wernlund

Støy

Lemming

et al. 2014

Scandinavian Journal of Infectious Diseases

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Acute alcoholic hepatitis (AH) is a life-threatening disease and its course is often determined by infections. However, the pattern of pathogens has not been studied. We examined the microbiological pathogens that caused blood-borne infection in patients with AH. We included 32 AH patients without infection at inclusion. Patients were followed for 1 month and their infection status was recorded based on clinical records, radiologic exams and cultures of different secreta. Nine patients (28%) developed blood culture-positive infections. The agents were of heterogeneous aetiology and came from various sites of infection. Candida species accounted for three of these infections (33%). Five patients (16%) died, two of which had positive blood cultures. A high fraction was invasively infected by a heterogeneous spectrum of microbes including yeasts and commensal bacteria. This may reflect the severe immune impairment of AH and suggests thorough infection screening and an immediate broad-spectrum antibiotic approach if infection is suspected.

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Alcohol takes the toll on immune function

Cited by 3 publications

References 19 publications

Expansion of Granulocytic, Myeloid-Derived Suppressor Cells in Response to Ethanol-Induced Acute Liver Damage

Expansion of Granulocytic, Myeloid-Derived Suppressor Cells in Response to Ethanol-Induced Acute Liver Damage

Bench-to-beside review: Acute-on-chronic liver failure - linking the gut, liver and systemic circulation

Blood culture-positive infections in patients with alcoholic hepatitis

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