{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T06:37:03Z","timestamp":1772087823226,"version":"3.50.1"},"reference-count":72,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T00:00:00Z","timestamp":1772064000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Zinc deficiency affects ~17% of the population globally, contributing to deficits in growth, metabolism and immunity. Serum zinc is greatly reduced in alcohol-associated hepatitis, driven by hepatic dysfunction and poor zinc retention. While zinc is an essential micronutrient with many beneficial anti-inflammatory and anti-oxidant properties, its role in the progression of alcohol-related liver disease (ALD) remains uncertain.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To identify broad transcriptomic responses to zinc, 11 publicly available datasets were examined to generate a transcriptomic zinc signature. Zinc signature genes were validated in vitro using primary immune cell and hepatocyte models supplemented with zinc or depleted of zinc using a S100A12 conjugated resin. The role of zinc deficiency in alcohol-associated hepatitis was examined bioinformatically, using large publicly available datasets, and confirmed\n                      <jats:italic>in vitro<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A nine gene zinc signature consisting primarily of metallothonein genes identified hepatic zinc deficiency among ALD patients that was associated with a down-regulation of the acute phase response pathway (e.g.,\n                      <jats:italic>SAA1, CRP<\/jats:italic>\n                      and\n                      <jats:italic>C9<\/jats:italic>\n                      genes).\n                      <jats:italic>In vitro<\/jats:italic>\n                      studies using hepatocyte and immune cell cultures depleted of zinc demonstrated that macrophage induction of the acute phase response by LPS was dampened by zinc depletion.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>Together, these data suggest that hepatic zinc stores among patients with alcohol-associated hepatitis are reduced, resulting in deficient acute-phase responses. Increasing hepatic zinc stores via supplementation and dietary modulation may improve acute responses to infection, and thus, long term outcomes in this patient group.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2025.1642163","type":"journal-article","created":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T05:28:52Z","timestamp":1772083732000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Hepatic zinc deficiency dampens the acute phase response in patients with alcohol-associated hepatitis"],"prefix":"10.3389","volume":"16","author":[{"given":"Scott A.","family":"Read","sequence":"first","affiliation":[{"name":"Blacktown Clinical School, Western Sydney University","place":["Blacktown, NSW, Australia"]},{"name":"Blacktown Hospital, Western Sydney Local Health District (WSLHD)","place":["Blacktown, NSW, Australia"]},{"name":"Storr Liver Centre, The Westmead Institute for Medical Research, 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