<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu T</submitter><funding>the National Key Research and Development Program of China</funding><funding>the Peking University Medicine Fund</funding><funding>The National Natural Science Foundation of China</funding><funding>Peking University Clinical + X</funding><pagination>4825</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9102452</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(9)</volume><pubmed_abstract>Alcohol liver disease (ALD) is characterized by intestinal barrier disruption and gut dysbiosis. Dysfunction of E74-like ETS transcription factor 4 (ELF4) leads to colitis. We aimed to test the hypothesis that intestinal ELF4 plays a critical role in maintaining the normal function of intestinal barrier and gut homeostasis in a mouse model of ALD. Intestinal ELF4 deficiency resulted in dysfunction of the intestinal barrier. &lt;i>Elf4&lt;sup>-/-&lt;/sup>&lt;/i> mice exhibited gut microbiota (GM) dysbiosis with the characteristic of a larger proportion of Proteobacteria. The LPS increased in &lt;i>Elf4&lt;sup>-/-&lt;/sup>&lt;/i> mice and was the most important differential metabolite between &lt;i>Elf4&lt;sup>-/-&lt;/sup>&lt;/i> mice and WT mice. Alcohol exposure increased liver-to-body weight ratio, and hepatic inflammation </pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Intestinal ELF4 Deletion Exacerbates Alcoholic Liver Disease by Disrupting Gut Homeostasis.</pubmed_title><pmcid>PMC9102452</pmcid><funding_grant_id>2020YFA0707800; 2016YFA0500300</funding_grant_id><funding_grant_id>PKU2020LCXQ009</funding_grant_id><funding_grant_id>31570891; 31872736; 32022028 and 81991505</funding_grant_id><pubmed_authors>Xie Y</pubmed_authors><pubmed_authors>Yang L</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Yu H</pubmed_authors><pubmed_authors>You F</pubmed_authors></additional><is_claimable>false</is_claimable><name>Intestinal ELF4 Deletion Exacerbates Alcoholic Liver Disease by Disrupting Gut Homeostasis.</name><description>Alcohol liver disease (ALD) is characterized by intestinal barrier disruption and gut dysbiosis. Dysfunction of E74-like ETS transcription factor 4 (ELF4) leads to colitis. We aimed to test the hypothesis that intestinal ELF4 plays a critical role in maintaining the normal function of intestinal barrier and gut homeostasis in a mouse model of ALD. Intestinal ELF4 deficiency resulted in dysfunction of the intestinal barrier. &lt;i>Elf4&lt;sup>-/-&lt;/sup>&lt;/i> mice exhibited gut microbiota (GM) dysbiosis with the characteristic of a larger proportion of Proteobacteria. The LPS increased in &lt;i>Elf4&lt;sup>-/-&lt;/sup>&lt;/i> mice and was the most important differential metabolite between &lt;i>Elf4&lt;sup>-/-&lt;/sup>&lt;/i> mice and WT mice. Alcohol exposure increased liver-to-body weight ratio, and hepatic inflammation </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2025-04-04T22:53:21.291Z</modification><creation>2025-02-19T00:55:56.746Z</creation></dates><accession>S-EPMC9102452</accession><cross_references><pubmed>35563234</pubmed><doi>10.3390/ijms23094825</doi></cross_references></HashMap>