{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T16:41:24Z","timestamp":1791477684298,"version":"4.3.4"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,9]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims:<\/jats:title>\n            <jats:p>Alcohol-perturbed gut immune homeostasis is associated with the development of alcoholic liver disease (ALD). However, the role of intestinal dendritic cells (DCs) in ALD progression is still unknown. This study aimed to investigate the cellular and molecular mechanisms through which intestinal DCs respond to alcohol exposure and contribute to the pathogenesis of ALD.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results:<\/jats:title>\n            <jats:p>After 8 weeks of alcohol consumption, the number of basic leucine zipper transcription factor ATF-like 3 (<jats:italic toggle=\"yes\">Batf3<\/jats:italic>)-dependent conventional type 1 DCs (cDC1s) was dramatically decreased in the intestine but not the liver. cDC1 deficient <jats:italic toggle=\"yes\">Batf3<\/jats:italic> knockout mice along with wild-type mice were subjected to chronic-binge ethanol feeding to determine the role of intestinal cDC1s reduction in ALD. cDC1s deficiency exacerbated alcohol-induced gut barrier disruption, bacterial endotoxin translocation into the circulation, and liver injury. Adoptive transfer of cDC1s to alcohol-fed mice ameliorated alcohol-mediated gut barrier dysfunction and liver injury. Further studies revealed that intestinal cDC1s serve as a positive regulator of <jats:italic toggle=\"yes\">Akkermansia muciniphila<\/jats:italic> (<jats:italic toggle=\"yes\">A. muciniphila<\/jats:italic>). Oral administration of <jats:italic toggle=\"yes\">A. muciniphila<\/jats:italic> markedly reversed alcoholic steatohepatitis in mice. Mechanistic studies revealed that cDC1s depletion exacerbated alcohol-downregulated intestinal antimicrobial peptides which play a crucial role in maintaining <jats:italic toggle=\"yes\">A. muciniphila<\/jats:italic> abundance, by disrupting the IL-12-interferon gamma signaling pathway. Lastly, we identified that intestinal cDC1s were required for the protective role of <jats:italic toggle=\"yes\">Lactobacillus reuteri<\/jats:italic> in alcoholic steatohepatitis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>This study demonstrated that cDC1s protect alcohol-induced liver injury by maintaining <jats:italic toggle=\"yes\">A. muciniphila<\/jats:italic> abundance in mice. Targeting cDC1s may serve as a promising therapeutic approach for treating ALD.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1097\/hep.0000000000000019","type":"journal-article","created":{"date-parts":[[2023,1,16]],"date-time":"2023-01-16T09:00:09Z","timestamp":1673859609000},"page":"896-910","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":31,"title":["Conventional type 1 dendritic cells protect against gut barrier disruption via maintaining Akkermansia muciniphila in alcoholic steatohepatitis"],"prefix":"10.1097","volume":"78","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5044-7711","authenticated-orcid":false,"given":"Liuyi","family":"Hao","sequence":"first","affiliation":[{"name":"Center for Translational Biomedical Research, Kannapolis, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Zhong","sequence":"additional","affiliation":[{"name":"Center for Translational Biomedical Research, Kannapolis, North Carolina, USA"},{"name":"Department of Nutrition, Kannapolis, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5569-9304","authenticated-orcid":false,"given":"Jongmin","family":"Woo","sequence":"additional","affiliation":[{"name":"Center for Translational Biomedical Research, Kannapolis, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyuan","family":"Wei","sequence":"additional","affiliation":[{"name":"Department of Animal Science, Division of Agriculture, University of Arkansas, Fayetteville, Arkansas, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, 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