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ABSTRACT: Background
Cardiac complications in patients with hypereosinophilia cause significant morbidity and mortality. However, mechanisms of how eosinophilic inflammation causes heart damage are poorly understood.Methods
We developed a model of hypereosinophilia-associated heart disease by challenging hypereosinophilic mice with a peptide from the cardiac myosin heavy chain. Disease outcomes were measured by histology, immunohistochemistry, flow cytometry, and measurement of cells and biomarkers in peripheral blood. Eosinophil dependence was determined by using eosinophil-deficient mice (ΔdblGATA). Single cells from the heart were subjected to single-cell RNA sequencing to assess cell composition, activation states, and expression profiles. In vitro studies used bone marrow
SUBMITTER: Sunusi U
PROVIDER: S-EPMC12491288 | biostudies-literature | 2025
REPOSITORIES: biostudies-literature