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.
Highlights
Some viruses, like coxsackie virus and hepatitis C virus, are known to cause viral myocarditis, as a cause for the subsequent development of dilated cardiomyopathy [1]
We investigated the effects of application of IL-13 treatment on cardiac Injury and protection of heart function in viral myocarditis as well as the involvement of macrophage polarization in the process
Mice were divided into 3 groups: Group 1, mice were injected with saline as a control for coxsackie virus B3 (CVB3) injection (Sham); Group 2, mice were injected with CVB3, but for control of IL13 administration, saline of same dose and frequency was given (CVB3); Group 3: mice were injected with CVB3 and IL-13 (CVB3+IL-13) (Figure 1A)
Summary
Like coxsackie virus and hepatitis C virus, are known to cause viral myocarditis, as a cause for the subsequent development of dilated cardiomyopathy [1]. Granulocyte colony-stimulating factor was often upregulated in myocarditis, suggesting activation of macrophages [7,8,9,10]. These evidence of involvement of cytokines in the pathogenesis of myocarditis led to the approaches of using inhibitory cytokines and cytokine suppression, e.g. IL-1 receptor antagonist or IL-10 [11], or suppressing IL-4 [12], in a cytokine therapy. Blockade of IL-4 partially suppresses the development of experimental viral myocarditis in A/J mice, suggesting involvement of Th2 cytokines in the pathology of viral myocarditis [12]. These characteristics determine a distinct function of IL13 from IL-4 during immune responses
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