{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T11:28:02Z","timestamp":1789385282752,"version":"build-2803163510"},"reference-count":37,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2016,6,30]],"date-time":"2016-06-30T00:00:00Z","timestamp":1467244800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Danish Council of Independent Research"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["APMIS"],"published-print":{"date-parts":[[2016,9]]},"abstract":"<jats:p>The role of sterile inflammation caused by release of damage\u2010associated molecular patterns (<jats:styled-content style=\"fixed-case\">DAMP<\/jats:styled-content>) remains unclear in human alcoholic hepatitis (<jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content>). The <jats:styled-content style=\"fixed-case\">DAMP<\/jats:styled-content>, high mobility group box\u20101 protein (<jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1) is released by tissue damage and inflammation. We aimed to investigate whether <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 is a primary inflammatory driver in <jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content> by determining <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 serum levels and effects on inflammatory cells from <jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content> patients. We measured serum <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 in 34 <jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content> patients and 10 healthy controls using <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>. Toll\u2010like receptor 4 (<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4) and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>14 expressions were assessed by flow cytometry on <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1\u2010stimulated peripheral blood mononuclear cells (<jats:styled-content style=\"fixed-case\">PBMC<\/jats:styled-content>) and <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content> was used to measure <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 in the supernatants. We observed 5\u2010fold higher serum levels of <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 in <jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content> patients at the day of diagnosis and day 30, but no associations to clinical outcome. <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 stimulation increased the expression of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 on <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>14+\u2010monocytes compared with unstimulated cells in the <jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content> patients. The <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1 and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 production in response to <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 was diminished in <jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content> patients. In conclusion, <jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content> patients have increased levels of <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 in their blood. This combined with an increased <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 expression, but an unaffected cytokine response to <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 suggest that <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>1 is not the primary driver of inflammation in <jats:styled-content style=\"fixed-case\">AH<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/apm.12568","type":"journal-article","created":{"date-parts":[[2016,6,30]],"date-time":"2016-06-30T11:37:10Z","timestamp":1467286630000},"page":"741-747","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["The damage\u2010associated molecular pattern HMGB1 is elevated in human alcoholic hepatitis, but does not seem to be a primary driver of inflammation"],"prefix":"10.1111","volume":"124","author":[{"given":"Tea 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