<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Sousa Oliveira CV</submitter><pubmed_abstract>Long after &lt;i>Trypanosoma cruzi&lt;/i> infection, 40% of individuals develop a progressive chronic chagasic cardiomyopathy (CCC), with systolic dysfunction and arrhythmias. Since we previously showed IL-1β mediates the development of systolic dysfunction and cardiac arrhythmias in diabetes mellitus and cardiorenal syndrome, and IL-1β remains elevated in Chagas disease patients, here we tested the role of IL-1β in CCC using a mouse model. Mice deficient in IL-1R expression (&lt;i>Il-1r&lt;sup>-/-&lt;/sup>&lt;/i> ) survived acute &lt;i>T. cruzi&lt;/i> infection with greater parasitemia than controls but did not lose weight as wild-type (WT) did. At the chronic stage, WT presented prolonged ventricular repolarization intervals (QJ), while &lt;i>Il-1r&lt;sup>-/-&lt;/sup>&lt;/i> presented intervals like noninfected controls. I</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1010257</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9627615</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IL-1β is not critical to chronic heart dysfunction in mice with Chagas disease.</pubmed_title><pmcid>PMC9627615</pmcid><pubmed_authors>Torres Bozza M</pubmed_authors><pubmed_authors>Mata-Santos H</pubmed_authors><pubmed_authors>Peroba Ramos I</pubmed_authors><pubmed_authors>Neto Paiva C</pubmed_authors><pubmed_authors>Figueiredo-Vanzan D</pubmed_authors><pubmed_authors>Sousa Oliveira CV</pubmed_authors><pubmed_authors>Moreno-Loaiza O</pubmed_authors><pubmed_authors>Medei E</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-1β is not critical to chronic heart dysfunction in mice with Chagas disease.</name><description>Long after &lt;i>Trypanosoma cruzi&lt;/i> infection, 40% of individuals develop a progressive chronic chagasic cardiomyopathy (CCC), with systolic dysfunction and arrhythmias. Since we previously showed IL-1β mediates the development of systolic dysfunction and cardiac arrhythmias in diabetes mellitus and cardiorenal syndrome, and IL-1β remains elevated in Chagas disease patients, here we tested the role of IL-1β in CCC using a mouse model. Mice deficient in IL-1R expression (&lt;i>Il-1r&lt;sup>-/-&lt;/sup>&lt;/i> ) survived acute &lt;i>T. cruzi&lt;/i> infection with greater parasitemia than controls but did not lose weight as wild-type (WT) did. At the chronic stage, WT presented prolonged ventricular repolarization intervals (QJ), while &lt;i>Il-1r&lt;sup>-/-&lt;/sup>&lt;/i> presented intervals like noninfected controls. I</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-21T16:49:33.274Z</modification><creation>2025-04-21T16:49:33.274Z</creation></dates><accession>S-EPMC9627615</accession><cross_references><pubmed>36341442</pubmed><doi>10.3389/fimmu.2022.1010257</doi></cross_references></HashMap>