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All\u2010trans retinoic acid (ATRA<\/jats:styled-content>), a VA<\/jats:styled-content>\u2010active metabolite, has anti\u2010inflammatory effects and its deficiency could contribute to the exacerbated proinflammatory reaction. The aim of this study was to investigate the effects of ATRA<\/jats:styled-content>\/VA<\/jats:styled-content> deficiency and supplementation on the monocyte response in ALD<\/jats:styled-content>.<\/jats:p><\/jats:sec>Methods<\/jats:title>Vitamin A and ATRA<\/jats:styled-content> plasma levels were quantified in ALD<\/jats:styled-content> patients and healthy subjects (HS<\/jats:styled-content>). The in vitro<\/jats:italic> effect of ATRA<\/jats:styled-content> on lipopolysaccharide (LPS<\/jats:styled-content>)\u2010induced TNF<\/jats:styled-content>\u2010\u03b1 production by human peripheral blood mononuclear cells (PBMC<\/jats:styled-content>) was assessed by ELISA<\/jats:styled-content> and RT<\/jats:styled-content>\u2010PCR<\/jats:styled-content>. The activation pattern of peritoneal macrophages (PerM\u03a6<\/jats:styled-content>) and circulating monocytes isolated from VA<\/jats:styled-content>\u2010deficient mice and ALD<\/jats:styled-content> patients, respectively, was evaluated by flow cytometry, quantification of TNF<\/jats:styled-content>\u2010\u03b1 and NO<\/jats:styled-content>2<\/jats:sub> production.<\/jats:p><\/jats:sec>Results<\/jats:title>Alcoholic liver disease patients (n<\/jats:italic>\u00a0=\u00a085) showed plasmatic VA<\/jats:styled-content> deficiency that was correlated with scores of severity and with the hepatic venous pressure gradient. ATRA<\/jats:styled-content> levels correlated significantly with VA<\/jats:styled-content> levels. In vitro<\/jats:italic>, ATRA<\/jats:styled-content> pretreatment decreased the overproduction of TNF<\/jats:styled-content>\u2010\u03b1 by LPS<\/jats:styled-content>\u2010stimulated PBMC<\/jats:styled-content> of ALD<\/jats:styled-content> patients. In vivo<\/jats:italic>, VA<\/jats:styled-content> deficiency in mice was associated with increased activation of PerM\u03a6<\/jats:styled-content>, while oral ATRA<\/jats:styled-content> supplementation normalized it.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>For the first time, we show that VA<\/jats:styled-content>\/ATRA<\/jats:styled-content> deficiencies in ALD<\/jats:styled-content> patients are associated with disease severity. Furthermore, our data strongly suggest that the VA<\/jats:styled-content> deficiency observed in ALD<\/jats:styled-content> patients might participate in the pathophysiology of the disease by priming immune cells, and that ATRA<\/jats:styled-content> supplementation could downregulate the deleterious proinflammatory state in cirrhosis and might thus be of therapeutic use.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.12249","type":"journal-article","created":{"date-parts":[[2013,6,19]],"date-time":"2013-06-19T11:53:49Z","timestamp":1371642829000},"page":"343-352","source":"Crossref","is-referenced-by-count":9,"title":["Correction of all\u2010trans retinoic acid deficiency in alcoholic cirrhosis lessens the excessive inflammatory monocyte response: a translational study"],"prefix":"10.1111","volume":"34","author":[{"given":"Romy","family":"Ouziel","sequence":"first","affiliation":[{"name":"Laboratory of Experimental Gastroenterology ULB Brussels Belgium"},{"name":"Department of 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