<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Wong SY</submitter><funding>Crohn&amp;apos;s and Colitis Foundation of America</funding><funding>American College of Gastroenterology</funding><funding>NIDDK NIH HHS</funding><funding>National Institute of Allergy and Infectious Diseases Division of Intramural Research</funding><funding>NIAID NIH HHS</funding><funding>Crohn&amp;apos;s and Colitis Foundation</funding><funding>NIH</funding><pagination>101533</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12506532</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>19(12)</volume><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>The role of goblet cells in small intestinal inflammation in Crohn's disease (CD) is unknown. Polymorphisms of NOD2 confer risk for CD and associate with small intestinal disease location. We previously showed in mice that Nod2 deficiency leads to overexpansion of Phocaeicola vulgatus in the gut and downstream goblet cell defects, which preceded small intestinal inflammation. In this study, we ask whether goblet cell defects occur in patients with CD with NOD2 polymorphisms and investigate in mice how Pvulgatus signals through the intestinal epithelium.&lt;h4>Methods&lt;/h4>We performed a retrospective study of patients with CD to assess clinical outcomes and goblet cell histology by NOD2 status. We evaluated the contribution of microbiota and MyD88 signaling in the int</pubmed_abstract><journal>Cellular and molecular gastroenterology and hepatology</journal><pubmed_title>Goblet Cell Loss Linked to NOD2 and Secondary Resection in Crohn's Disease Is Induced by Dysbiosis and Epithelial MyD88.</pubmed_title><pmcid>PMC12506532</pmcid><funding_grant_id>R01 DK103788</funding_grant_id><funding_grant_id>R01 AI130945</funding_grant_id><pubmed_authors>Jang KK</pubmed_authors><pubmed_authors>Yang H</pubmed_authors><pubmed_authors>Estevinho MM</pubmed_authors><pubmed_authors>Cadwell K</pubmed_authors><pubmed_authors>Giselbrecht E</pubmed_authors><pubmed_authors>Lewis JD</pubmed_authors><pubmed_authors>Paulsen JD</pubmed_authors><pubmed_authors>Bittinger K</pubmed_authors><pubmed_authors>Daniel SG</pubmed_authors><pubmed_authors>Wong SY</pubmed_authors><pubmed_authors>Ko HM</pubmed_authors><pubmed_authors>Ding Y</pubmed_authors><pubmed_authors>Cho JH</pubmed_authors><pubmed_authors>Zhou C</pubmed_authors><pubmed_authors>Rosas-Villegas A</pubmed_authors><pubmed_authors>Ramanan D</pubmed_authors><pubmed_authors>Marshall AA</pubmed_authors><pubmed_authors>Heaney T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Goblet Cell Loss Linked to NOD2 and Secondary Resection in Crohn's Disease Is Induced by Dysbiosis and Epithelial MyD88.</name><description>&lt;h4>Background &amp; aims&lt;/h4>The role of goblet cells in small intestinal inflammation in Crohn's disease (CD) is unknown. Polymorphisms of NOD2 confer risk for CD and associate with small intestinal disease location. We previously showed in mice that Nod2 deficiency leads to overexpansion of Phocaeicola vulgatus in the gut and downstream goblet cell defects, which preceded small intestinal inflammation. In this study, we ask whether goblet cell defects occur in patients with CD with NOD2 polymorphisms and investigate in mice how Pvulgatus signals through the intestinal epithelium.&lt;h4>Methods&lt;/h4>We performed a retrospective study of patients with CD to assess clinical outcomes and goblet cell histology by NOD2 status. We evaluated the contribution of microbiota and MyD88 signaling in the int</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-07-15T14:31:56.339Z</modification><creation>2026-07-06T03:08:52.043Z</creation></dates><accession>S-EPMC12506532</accession><cross_references><pubmed>40378921</pubmed><doi>10.1016/j.jcmgh.2025.101533</doi></cross_references></HashMap>