Abstract
Previous studies have indicated that heavy alcohol intake stimulates inflammation and impairs the body's ability to regulate inflammation. The aim of this study was to compare changes in neutrophil calprotectin and a wide spectrum of other inflammatory mediators in response to heavy alcohol drinking. Serum calprotectin (a marker of neutrophil activation), suPAR, CD163, and pro- (IL-6, IL-8, TNF-α) and anti-inflammatory (IL-10, TGF-β) cytokines were measured from 61 alcohol-dependent subjects (46 men, 15 women, mean age 43.6±11.0 years) at the time of admission for detoxification and after 8±2 days of abstinence. These biomarkers were also measured from age- and sex-matched healthy controls representing abstainers or light drinkers. The clinical assessments included detailed clinical interviews on the amounts and patterns of alcohol consumption and assays for biomarkers of alcohol consumption (GGT, CDT, MCV, GGT-CDT) and liver function (AST, ALT). The subjects with alcohol use disorder showed significantly higher concentrations of serum calprotectin (p<0.0005), suPAR (p<0.01), CD163 (p<0.01), IL-6 (p<0.0005), IL-8 (p<0.0005), TNF-α (p<0.001), and IL-10 (p<0.0005) than healthy controls. These inflammatory mediators, except for CD163, remained elevated after the 8 ± 2-day period of supervised abstinence, which resulted in significant decreases in the biomarkers of alcohol consumption and indices of liver status. The AUC (0.855) for serum calprotectin in differentiating between the heavy drinkers and healthy controls was equal or equivalent with those of the conventional biomarkers of alcohol consumption (GGT:0.835 or CDT:0.803). The data indicate that neutrophil calprotectin is released in response to heavy alcohol intake in a sensitive manner and may be associated with perpetuation of inflammation in patients with alcohol use disorder. Serum calprotectin may also prove to be a useful biomarker for inflammatory activity in alcohol-consuming patients.
Highlights
IntroductionExcessive systemic inflammation and immune dysfunction have been suggested to play a pivotal role in the sequence of events leading to tissue injury in patients with alcohol use disorder AbbreviationsALT AST CD163 CDT GGT IL suPARTGF-b TNF-a alanine aminotransferase aspartate aminotransferase a biomarker of monocyte-macrophage activation carbohydrate-deficient transferrin gamma glutamyl transferase interleukin soluble urokinase plasminogen activator receptor, a biomarker of immune activation transforming growth factor-beta tumor necrosis factor-alpha have suggested that the shifts in immune mediators may occur in an alcohol-dose dependent manner (Sureshchandra et al, 2019).While a wide spectrum of new and emerging serum inflammatory biomarkers have recently been made available, as yet only limited information has been available on simultaneous comparisons of responses in the mediators of inflammation following heavy alcohol intake
Soluble urokinase plasminogen activator and CD163 are proteins which have recently emerged as possible prospective risk factors for adverse clinical outcomes in inflammatory conditions (Andersen, Eugen-Olsen, Kofoed, Iversen, & Haugaard, 2008; Buehler et al, 2009; Koch et al, 2011; Møller, 2012; Thunø, Macho, & Eugen-Olsen, 2009). soluble urokinase plasminogen activator (suPAR) is expressed on many immunologically active cells, including monocytes, neutrophils, and activated T cells (Andersen et al, 2008; Koch et al, 2011; Thunø et al, 2009), whereas CD163 is found on macrophages and monocytes
To gain further insight on the changes in the status of inflammation and neutrophil activation in response to heavy alcohol intake, we compared the responses in serum calprotectin with those of a wide variety of other immune mediators, including suPAR, CD163, pro- (IL-6, IL-8, TNF-a) and anti-inflammatory (IL-10, TGF-b) cytokines and conventional biomarkers of alcohol consumption and liver status from alcohol-dependent subjects at the time of admission for detoxification and after an 8 ± 2 day period of supervised abstinence
Summary
Excessive systemic inflammation and immune dysfunction have been suggested to play a pivotal role in the sequence of events leading to tissue injury in patients with alcohol use disorder AbbreviationsALT AST CD163 CDT GGT IL suPARTGF-b TNF-a alanine aminotransferase aspartate aminotransferase a biomarker of monocyte-macrophage activation carbohydrate-deficient transferrin gamma glutamyl transferase interleukin soluble urokinase plasminogen activator receptor, a biomarker of immune activation transforming growth factor-beta tumor necrosis factor-alpha have suggested that the shifts in immune mediators may occur in an alcohol-dose dependent manner (Sureshchandra et al, 2019).While a wide spectrum of new and emerging serum inflammatory biomarkers have recently been made available, as yet only limited information has been available on simultaneous comparisons of responses in the mediators of inflammation following heavy alcohol intake. To gain further insight on the changes in the status of inflammation and neutrophil activation in response to heavy alcohol intake, we compared the responses in serum calprotectin with those of a wide variety of other immune mediators, including suPAR, CD163, pro- (IL-6, IL-8, TNF-a) and anti-inflammatory (IL-10, TGF-b) cytokines and conventional biomarkers of alcohol consumption and liver status from alcohol-dependent subjects at the time of admission for detoxification and after an 8 ± 2 day period of supervised abstinence These parameters were measured from age- and sex-matched control subjects representing apparently healthy abstainers or light drinkers
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