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.
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This study was funded by the National Natural Science Foundation of China (81670345).
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Li, Y., Huang, Y., Wu, W. et al. B Cells Increase Myocardial Inflammation by Suppressing M2 Macrophage Polarization in Coxsackie Virus B3-Induced Acute Myocarditis. Inflammation 42, 953–960 (2019). https://doi.org/10.1007/s10753-018-0950-0
- B cells
- viral myocarditis