B Cells Increase Myocardial Inflammation by Suppressing M2 Macrophage Polarization in Coxsackie Virus B3-Induced Acute Myocarditis

  • Yong Li
  • Yanlan Huang
  • Weifeng WuEmail author
  • Bin Wei
  • Lin Qin


The role of B cells in viral myocarditis (VMC) remains controversial. In order to establish a role and mechanism of action for B cells in acute VMC, we established an acute VMC mouse model by intraperitoneal injection of Coxsackie virus group B type 3 (CVB3). At day 7, mice were analyzed using myocardial histopathology, and the presence of M2 macrophages in spleen and heart. Mice were divided into four groups, all having a C57BL/6 background: control group; wild-type (WT) VMC; mMt/mMt (−/−) VMC (BKO), and BKO + B cell VMC. A role for B cells was demonstrated by a significant reduction in myocardial pathological score and an increase in the frequency of M2 macrophages in the BKO group, when compared to the WT group. Once BKO mice underwent B cell reconstitution with isolated WT B cells, the myocardial pathological score was increased significantly, while the frequency of M2 macrophages decrease. Our findings demonstrate that B cells increase myocardial inflammation by suppressing M2 polarization in acute VMC in vivo.


B cells macrophage polarization viral myocarditis 


Funding Information

This study was funded by the National Natural Science Foundation of China (81670345).

Compliance with Ethical Standards

Conflict of Interest

The authors declare that they have no conflicts of interest.


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© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of CardiologyFirst Affiliated Hospital of Guangxi Medical UniversityNanningPeople’s Republic of China

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