<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zubeldia-Varela E</submitter><funding>Japan Society for the Promotion of Science (JSPS)</funding><funding>Deutscher Akademischer Austausch Dienst (DAAD)</funding><funding>FEDER 'Investing in your future' for the thematic network and co-operative research centres RICORS 'Red de Enfermedades Inflamatorias (REI)'</funding><funding>Instituto de Salud Carlos III</funding><funding>European Regional Development Fund</funding><pagination>3430-3447</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11657046</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>79(12)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The pathological mechanism of the gastrointestinal forms of food allergies is less understood in comparison to other clinical phenotypes, such as asthma and anaphylaxis Importantly, high-IgE levels are a poor prognostic factor in gastrointestinal allergies.&lt;h4>Methods&lt;/h4>This study investigated how high-IgE levels influence the development of intestinal inflammation and the metabolome in allergic enteritis (AE), using IgE knock-in (IgEki) mice expressing high levels of IgE. In addition, correlation of the altered metabolome with gut microbiome was analysed.&lt;h4>Results&lt;/h4>Ovalbumin-sensitized and egg-white diet-fed (OVA/EW) BALB/c WT mice developed moderate AE, whereas OVA/EW IgEki mice induced more aggravated intestinal inflammation with enhanced eosinophil accumulatio</pubmed_abstract><journal>Allergy</journal><pubmed_title>The impact of high-IgE levels on metabolome and microbiome in experimental allergic enteritis.</pubmed_title><pmcid>PMC11657046</pmcid><funding_grant_id>PI19/00044</funding_grant_id><funding_grant_id>(RD21/0002/0008)</funding_grant_id><funding_grant_id>PI20/01366</funding_grant_id><funding_grant_id>PID2021‐122490NB‐I00</funding_grant_id><funding_grant_id>PI17/01087</funding_grant_id><funding_grant_id>PID2021-122490NB-I00</funding_grant_id><pubmed_authors>Vieths S</pubmed_authors><pubmed_authors>Barbas C</pubmed_authors><pubmed_authors>Perez-Gordo M</pubmed_authors><pubmed_authors>Gonzalez-Menendez I</pubmed_authors><pubmed_authors>Martella M</pubmed_authors><pubmed_authors>Nochi T</pubmed_authors><pubmed_authors>Laino J</pubmed_authors><pubmed_authors>Yu P</pubmed_authors><pubmed_authors>Barber D</pubmed_authors><pubmed_authors>Toda M</pubmed_authors><pubmed_authors>Steigerwald H</pubmed_authors><pubmed_authors>Quintanilla-Martinez L</pubmed_authors><pubmed_authors>Krause M</pubmed_authors><pubmed_authors>Zubeldia-Varela E</pubmed_authors><pubmed_authors>Islam J</pubmed_authors><pubmed_authors>Blanco-Perez F</pubmed_authors><pubmed_authors>Barker-Tejeda TC</pubmed_authors><pubmed_authors>Rojo D</pubmed_authors><pubmed_authors>Villasenor A</pubmed_authors></additional><is_claimable>false</is_claimable><name>The impact of high-IgE levels on metabolome and microbiome in experimental allergic enteritis.</name><description>&lt;h4>Background&lt;/h4>The pathological mechanism of the gastrointestinal forms of food allergies is less understood in comparison to other clinical phenotypes, such as asthma and anaphylaxis Importantly, high-IgE levels are a poor prognostic factor in gastrointestinal allergies.&lt;h4>Methods&lt;/h4>This study investigated how high-IgE levels influence the development of intestinal inflammation and the metabolome in allergic enteritis (AE), using IgE knock-in (IgEki) mice expressing high levels of IgE. In addition, correlation of the altered metabolome with gut microbiome was analysed.&lt;h4>Results&lt;/h4>Ovalbumin-sensitized and egg-white diet-fed (OVA/EW) BALB/c WT mice developed moderate AE, whereas OVA/EW IgEki mice induced more aggravated intestinal inflammation with enhanced eosinophil accumulatio</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2025-04-18T14:40:12.11Z</modification><creation>2025-04-07T00:56:43.927Z</creation></dates><accession>S-EPMC11657046</accession><cross_references><pubmed>38932655</pubmed><doi>10.1111/all.16202</doi></cross_references></HashMap>