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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.

Original publication




Journal article


Jacc basic transl sci

Publication Date





665 - 681


BMD, bone marrow derived, IL, interleukin, MI, myocardial infarction, PBS, phosphate-buffered saline, STEMI, STEMI, ST-segment elevation myocardial infarction, WT, wild-type, eosinophil, mRNA, messenger RNA, qPCR, quantitative polymerase chain reaction, remodeling