<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hahn L</submitter><funding>Deutsche Forschungsgemeinschaft</funding><funding>Interdisciplinary Centre for Clinical Research within the Faculty of Medicine at the RWTH Aachen University</funding><funding>Von-Behring-Röntgen-Stiftung</funding><pagination>E1949</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7564366</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9(9)</volume><pubmed_abstract>The Th2 cytokine IL-13 is involved in biliary epithelial injury and liver fibrosis in patients as well as in animal models. The aim of this study was to investigate IL-13 as a therapeutic target during short term and chronic intrahepatic cholestasis in an &lt;i>Abcb4-&lt;/i>knockout mouse model (&lt;i>Abcb4&lt;/i>&lt;sup>-/-&lt;/sup>). Lack of IL-13 protected &lt;i>Abcb4&lt;/i>&lt;sup>-/-&lt;/sup> mice transiently from cholestasis. This decrease in serum bile acids was accompanied by an enhanced excretion of bile acids and a normalization of fecal bile acid composition. In &lt;i>Abcb4&lt;sup>-/-&lt;/sup>/IL-13&lt;/i>&lt;sup>-/-&lt;/sup> double knockout mice, bacterial translocation to the liver was significantly reduced and the intestinal microbiome resembled the commensal composition in wild type animals. In addition, 52-week-old &lt;i>Ab</pubmed_abstract><journal>Cells</journal><pubmed_title>IL-13 as Target to Reduce Cholestasis and Dysbiosis in &lt;i>Abcb4&lt;/i> Knockout Mice.</pubmed_title><pmcid>PMC7564366</pmcid><funding_grant_id>SFB1021 Z02</funding_grant_id><funding_grant_id>KFO309 Z01</funding_grant_id><funding_grant_id>KFO 217</funding_grant_id><funding_grant_id>RO 957/10-1</funding_grant_id><funding_grant_id>project O3-1</funding_grant_id><funding_grant_id>RO 3714/4</funding_grant_id><funding_grant_id>SFB/TRR57, projects P13 and Q3</funding_grant_id><funding_grant_id>60-0002</funding_grant_id><funding_grant_id>SFB-TR84 project B08</funding_grant_id><funding_grant_id>RO 957/11</funding_grant_id><pubmed_authors>Mayatepek E</pubmed_authors><pubmed_authors>Baier A</pubmed_authors><pubmed_authors>Drebber U</pubmed_authors><pubmed_authors>Weiskirchen R</pubmed_authors><pubmed_authors>Weigel M</pubmed_authors><pubmed_authors>Helmrich N</pubmed_authors><pubmed_authors>Windhorst A</pubmed_authors><pubmed_authors>Roeb E</pubmed_authors><pubmed_authors>Domann E</pubmed_authors><pubmed_authors>Rath T</pubmed_authors><pubmed_authors>Hahn L</pubmed_authors><pubmed_authors>Olejniczak S</pubmed_authors><pubmed_authors>Schmidt N</pubmed_authors><pubmed_authors>Ewers C</pubmed_authors><pubmed_authors>Churin Y</pubmed_authors><pubmed_authors>Hain T</pubmed_authors><pubmed_authors>Mollenkopf HJ</pubmed_authors><pubmed_authors>Roderfeld M</pubmed_authors><pubmed_authors>Herebian D</pubmed_authors><pubmed_authors>Steinhoff U</pubmed_authors><pubmed_authors>Wirtz S</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-13 as Target to Reduce Cholestasis and Dysbiosis in &lt;i>Abcb4&lt;/i> Knockout Mice.</name><description>The Th2 cytokine IL-13 is involved in biliary epithelial injury and liver fibrosis in patients as well as in animal models. The aim of this study was to investigate IL-13 as a therapeutic target during short term and chronic intrahepatic cholestasis in an &lt;i>Abcb4-&lt;/i>knockout mouse model (&lt;i>Abcb4&lt;/i>&lt;sup>-/-&lt;/sup>). Lack of IL-13 protected &lt;i>Abcb4&lt;/i>&lt;sup>-/-&lt;/sup> mice transiently from cholestasis. This decrease in serum bile acids was accompanied by an enhanced excretion of bile acids and a normalization of fecal bile acid composition. In &lt;i>Abcb4&lt;sup>-/-&lt;/sup>/IL-13&lt;/i>&lt;sup>-/-&lt;/sup> double knockout mice, bacterial translocation to the liver was significantly reduced and the intestinal microbiome resembled the commensal composition in wild type animals. In addition, 52-week-old &lt;i>Ab</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Aug</publication><modification>2026-04-14T23:20:28.552Z</modification><creation>2020-10-30T08:35:14Z</creation></dates><accession>S-EPMC7564366</accession><cross_references><pubmed>32846954</pubmed><doi>10.3390/cells9091949</doi></cross_references></HashMap>