<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16(1)</volume><submitter>Fargeas M</submitter><funding>Agence Nationale de la Recherche</funding><pubmed_abstract>We investigated the role of ChiA and its associated polymorphisms in the interaction between Crohn's disease (CD)-associated adherent-invasive &lt;i>Escherichia coli&lt;/i> (AIEC) and intestinal mucosa. We observed a higher abundance of &lt;i>chiA&lt;/i> among the metagenome of CD patients compared to healthy subjects. In dextran sulfate sodium-induced colitis mice model, AIEC-LF82∆&lt;i>chiA&lt;/i> colonization was reduced in ileal, colonic and fecal samples compared to wild-type LF82. The binding of ChiA to recombinant human CHI3L1 or mucus was higher with the pathogenic polymorphism. The strength of ChiA-mucin interaction was 300-fold stronger than ChiA-rhCHI3L1. ChiA was able to degrade mucin to promote its growth and enabled LF82 to get closer to epithelial cells. The pathogenic polymorphism of ChiA ha</pubmed_abstract><journal>Gut microbes</journal><pagination>2412667</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11486038</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>ChiA: a major player in the virulence of Crohn's disease-associated adherent and invasive &lt;i>Escherichia coli&lt;/i> (AIEC).</pubmed_title><pmcid>PMC11486038</pmcid><pubmed_authors>Faure F</pubmed_authors><pubmed_authors>Denizot J</pubmed_authors><pubmed_authors>Buisson A</pubmed_authors><pubmed_authors>Chevarin C</pubmed_authors><pubmed_authors>Birer A</pubmed_authors><pubmed_authors>Billard E</pubmed_authors><pubmed_authors>Barnich N</pubmed_authors><pubmed_authors>Fargeas M</pubmed_authors><pubmed_authors>Rodrigues M</pubmed_authors><pubmed_authors>Douadi C</pubmed_authors><pubmed_authors>Sivignon A</pubmed_authors></additional><is_claimable>false</is_claimable><name>ChiA: a major player in the virulence of Crohn's disease-associated adherent and invasive &lt;i>Escherichia coli&lt;/i> (AIEC).</name><description>We investigated the role of ChiA and its associated polymorphisms in the interaction between Crohn's disease (CD)-associated adherent-invasive &lt;i>Escherichia coli&lt;/i> (AIEC) and intestinal mucosa. We observed a higher abundance of &lt;i>chiA&lt;/i> among the metagenome of CD patients compared to healthy subjects. In dextran sulfate sodium-induced colitis mice model, AIEC-LF82∆&lt;i>chiA&lt;/i> colonization was reduced in ileal, colonic and fecal samples compared to wild-type LF82. The binding of ChiA to recombinant human CHI3L1 or mucus was higher with the pathogenic polymorphism. The strength of ChiA-mucin interaction was 300-fold stronger than ChiA-rhCHI3L1. ChiA was able to degrade mucin to promote its growth and enabled LF82 to get closer to epithelial cells. The pathogenic polymorphism of ChiA ha</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jan-Dec</publication><modification>2026-07-01T03:10:19.683Z</modification><creation>2025-04-04T01:54:06.726Z</creation></dates><accession>S-EPMC11486038</accession><cross_references><pubmed>39397494</pubmed><doi>10.1080/19490976.2024.2412667</doi></cross_references></HashMap>