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Interleukin\u201033 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033) acts as a danger\u2010associated molecular pattern (<jats:styled-content style=\"fixed-case\">DAMP<\/jats:styled-content>) to modulate immune response. However, the role of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 in regulating monocyte function during hepatitis B\u2010precipitated <jats:styled-content style=\"fixed-case\">ACLF<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ACLF<\/jats:styled-content>) in response to lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>) has not been clear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>In this study, the levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033\/<jats:styled-content style=\"fixed-case\">ST<\/jats:styled-content>2 in blood and liver samples collected from patients with <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ACLF<\/jats:styled-content>, chronic hepatitis B (<jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content>) and normal controls and the associated of those findings with disease severity were analysed. <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>80 expression, phagocytosis capacity, cytokine secretion and <jats:styled-content style=\"fixed-case\">MAP<\/jats:styled-content> kinase activation induced by <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> were detected to explore the role of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033\/<jats:styled-content style=\"fixed-case\">ST<\/jats:styled-content>2 signal in regulating monocyte function in patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The expression levels of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033\/<jats:styled-content style=\"fixed-case\">ST<\/jats:styled-content>2 were significantly increased in peripheral blood and livers of patients with <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ACLF<\/jats:styled-content>, as compared with patients with <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> and controls. It was found that serum <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 level was associated with severity of liver disease. Treatment with <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 on monocytes significantly increased <jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DR<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> CCR<\/jats:styled-content>2 and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>80 expression, enhanced <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010stimulated <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 secretion, but did not affect the phagocytic capacity. Furthermore, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 signalling enhanced the <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>1\/2 activation of monocytes in response to <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">DAMP<\/jats:styled-content> molecular <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201033 augmented the \u2018storm\u2019 of monocytic inflammation in response to <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> through <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>1\/2 activation during <jats:styled-content style=\"fixed-case\">HB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ACLF<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.13503","type":"journal-article","created":{"date-parts":[[2017,6,22]],"date-time":"2017-06-22T14:46:44Z","timestamp":1498142804000},"page":"229-238","source":"Crossref","is-referenced-by-count":40,"title":["<scp>DAMP<\/scp> molecular <scp>IL<\/scp>\u201033 augments monocytic inflammatory storm in hepatitis B\u2010precipitated acute\u2010on\u2010chronic liver failure"],"prefix":"10.1111","volume":"38","author":[{"given":"Xing X.","family":"Du","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases Sir Run Run Shaw Hospital School of Medicine Zhejiang University  Hangzhou Zhejiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9392-7176","authenticated-orcid":false,"given":"Yu","family":"Shi","sequence":"additional","affiliation":[{"name":"State Key Laboratory for Diagnosis and Treatment of Infectious Diseases 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