B Cells Increase Myocardial Inflammation by Suppressing M2 Macrophage Polarization in Coxsackie Virus B3-Induced Acute Myocarditis
B Cells Increase Myocardial Inflammation by Suppressing M2 Macrophage Polarization in Coxsackie Virus B3-Induced Acute Myocarditis
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在柯萨奇病毒 B3 诱发的急性心肌炎中，B 细胞通过抑制 M2 巨噬细胞极化来增加心肌炎症
DOI：
10.1007/s10753-018-0950-0
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发表时间：
2019-06-01
期刊：
影响因子：
5.1
通讯作者：
Qin, Lin
中科院分区：
文献类型：
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作者：
Li, Yong;Huang, Yanlan;Qin, Lin
B细胞在病毒性心肌炎（VMC）中的作用仍存在争议。为探讨B细胞在急性病毒性心肌炎中的作用及机制，我们采用科萨基病毒B 3型（CVB 3）腹腔注射建立急性病毒性心肌炎小鼠模型。第7天，使用心肌组织病理学以及脾脏和心脏中M2巨噬细胞的存在来分析小鼠。将小鼠分为四组，均具有C57 BL/6背景：对照组;野生型（WT）VMC; mMt/mMt（-/-）VMC（BKO）和BKO + B细胞VMC。与WT组相比，BKO组心肌病理评分显著降低，M2巨噬细胞频率增加，证明了B细胞的作用。一旦BKO小鼠接受分离的WT B细胞重建B细胞，心肌病理评分显著增加，而M2巨噬细胞的频率减少。我们的研究结果表明，B细胞通过抑制M2极化在急性VMC中增加心肌炎症。
AbstractThe 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 VMCin vivo.