Interleukin-13 reduces cardiac injury and prevents heart dysfunction in viral myocarditis via enhanced M2 macrophage polarization

Abstract

Viral myocarditis is one of the major causes of congestive heart failure and dilated cardiomyopathy. Recent reports have demonstrated an essential role of cytokines, like interleukin-13 (IL-13), in the pathogenesis of viral myocarditis, while the underlying mechanisms remain poorly defined. Here, using a coxsackie virus B3 (CVB3)-infection model in BALB/C mice, we showed that IL-13 protected mouse heart function in viral myocarditis, seemingly through reduction in T lymphocyte immunity and induction of M2 macrophage polarization. Adoptive transfer to M2 macrophages mimicked the effects of IL-13 on protection from myocarditis, suggesting that the effects of IL-13 may be primarily through regulation of macrophage polarization. Together, our data suggest that application of IL-13 treatment may reduce cardiac Injury and protect heart function in viral myocarditis via enhanced M2 macrophage polarization.