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Eosinophil Deficiency Promotes Aberrant Repair and Adverse Remodeling Following Acute Myocardial InfarctionOpen Access

Clinical Research

J Am Coll Cardiol Basic Trans Science, 5 (7) 665–681
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Highlights

A drop in eosinophil blood count is associated with recruitment of eosinophils to the heart during repair following clinical and experimental MI.

Genetic and pharmacological eosinophil depletion leads to increased adverse remodeling in experimental MI.

Eosinophils are required for acquisition of an anti-inflammatory macrophage phenotype, a shift to resolution of inflammation and mature scar formation during infarct repair.

IL-4 therapy is able to rescue the adverse remodeling phenotype in conditions of eosinophil deficiency.

Summary

In ST-segment elevation myocardial infarction of both patients and mice, there was a decline in blood eosinophil count, with activated eosinophils recruited to the infarct zone. Eosinophil deficiency resulted in attenuated anti-inflammatory macrophage polarization, enhanced myocardial inflammation, increased scar size, and deterioration of myocardial structure and function. Adverse cardiac remodeling in the setting of eosinophil deficiency was prevented by interleukin-4 therapy.

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