Eosinophil Deficiency Promotes Aberrant Repair and Adverse Remodeling Following Acute Myocardial Infarction
Clinical Research
Visual Abstract
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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