Hypereosinophilia causes progressive cardiac pathologies in mice

Nicola Laura Diny, Megan Kay Wood, Taejoon Won, Monica Vladut Talor, Clarisse Lukban, Djahida Bedja, Nadan Wang, Hannah Kalinoski, Abdel Daoud, C. Conover Talbot, Brian Leei Lin, Daniela Čiháková

Research output: Contribution to journalArticlepeer-review


Hypereosinophilic syndrome is a progressive disease with extensive eosinophilia that results in organ damage. Cardiac pathologies are the main reason for its high mortality rate. A better understanding of the mechanisms of eosinophil-mediated tissue damage would benefit therapeutic development. Here, we describe the cardiac pathologies that developed in a mouse model of hypereosinophilic syndrome. These IL-5 transgenic mice exhibited decreased left ventricular function at a young age which worsened with age. Mechanistically, we demonstrated infiltration of activated eosinophils into the heart tissue that led to an inflammatory environment. Gene expression signatures showed tissue damage as well as repair and remodeling processes. Cardiomyocytes from IL-5Tg mice exhibited significantly reduced contractility relative to wild type (WT) controls. This impairment may result from the inflammatory stress experienced by the cardiomyocytes and suggest that dysregulation of contractility and Ca2+ reuptake in cardiomyocytes contributes to cardiac dysfunction at the whole organ level in hypereosinophilic mice.

Original languageEnglish (US)
Article number107990
Issue number10
StatePublished - Oct 20 2023
Externally publishedYes


  • Cell biology
  • Molecular biology
  • Physiology

ASJC Scopus subject areas

  • General


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