Despite the functions of TLRs in the parasitic infections have been extensively reported, few studies have addressed the role of TLR3 in the immune response to Schistosoma japonicum infections. The aim of this study was to investigate the properties of TLR3 in the liver of C57BL/6 mice infected by S. japonicum. The production of TLR3+ cells in CD4+T cells (CD4+CD3+), CD8+T cells (CD8+CD3+), γδT cells (γδTCR+CD3+), NKT cells (NK1.1+CD3+), B cells (CD19+CD3−), NK (NK1.1−CD3+) cells, MDSC (CD11b+Gr1+), macrophages (CD11b+F4/80+), DCs (CD11c+CD11b+) and neutrophils (CD11b+ Ly6g+) were assessed by flow cytometry. Sections of the liver were examined by haematoxylin and eosin staining in order to measure the area of granulomas. Hematological parameters including white blood cell (WBC), red blood cell (RBC), platelet (PLT) and hemoglobin (HGB) were analyzed. The levels of ALT and AST in the serum were measured using biochemical kits. The relative titers of anti-SEA IgG and anti-SEA IgM in the serum were measured by enzyme-linked immunosorbent assay (ELISA). CD25, CD69, CD314 and CD94 molecules were detected by flow cytometry. Flow cytometry results showed that the expression of TLR3 increased significantly after S. japonicum infection (P < 0.05). Hepatic myeloid and lymphoid cells could express TLR3, and the percentages of TLR3-expressing MDSC, macrophages and neutrophils were increased after infection. Knocking out TLR3 ameliorated the damage and decreased infiltration of inflammatory cells in infected C57BL/6 mouse livers.,The number of WBC was significantly reduced in TLR3 KO-infected mice compared to WT-infected mice (P < 0.01), but the levels of RBC, platelet and HGB were significantly increased in KO infected mice. Moreover, the relative titers of anti-SEA IgG and anti-SEA IgM in the serum of infected KO mice were statistically decreased compared with the infected WT mice. We also compared the activation-associated molecules expression between S.japonicum-infected WT and TLR3 KO mice. Taken together, our data indicated that TLR3 played potential roles in the context of S. japonicum infection and it may accelerate the progression of S. japonicum-associated liver pathology.

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日本血吸虫引起的病理过程中 TLR3 参与的评估

尽管 TLR 在寄生虫感染中的功能已被广泛报道，但很少有研究探讨 TLR3 在日本血吸虫感染免疫反应中的作用。本研究的目的是研究感染日本血吸虫的 C57BL/6 小鼠肝脏中 TLR3 的特性。CD4+T细胞(CD4+CD3+)、CD8+T细胞(CD8+CD3+)、γδT细胞(γδTCR+CD3+)、NKT细胞(NK1.1+CD3+)、B细胞(CD19+CD3)中TLR3+细胞的产生−)、NK (NK1.1−CD3+) 细胞、MDSC (CD11b+Gr1+)、巨噬细胞 (CD11b+F4/80+)、DC (CD11c+CD11b+) 和中性粒细胞 (CD11b+ Ly6g+) 通过流式细胞术进行评估。通过苏木精和伊红染色检查肝脏切片以测量肉芽肿的面积。分析血液学参数，包括白细胞（WBC）、红细胞（RBC）、血小板（PLT）和血红蛋白（HGB）。使用生化试剂盒测定血清中 ALT 和 AST 的水平。采用酶联免疫吸附试验（ELISA）测定血清中抗SEA IgG和抗SEA IgM的相对滴度。通过流式细胞术检测CD25、CD69、CD314和CD94分子。流式细胞术结果显示，日本血吸虫感染后TLR3表达显着升高（P < 0.05）。肝髓系和淋巴细胞可表达TLR3，感染后表达TLR3的MDSC、巨噬细胞和中性粒细胞百分比增加。敲除 TLR3 可改善 C57BL/6 感染小鼠肝脏的损伤并减少炎症细胞浸润。与 WT 感染小鼠相比，TLR3 KO 感染小鼠的 WBC 数量显着减少（P < 0.01），但KO感染小鼠的红细胞、血小板和HGB显着增加。此外，与感染的WT小鼠相比，感染的KO小鼠血清中抗SEA IgG和抗SEA IgM的相对滴度有统计学意义的降低。我们还比较了日本血吸虫感染的 WT 和 TLR3 KO 小鼠之间的激活相关分子表达。总而言之，我们的数据表明，TLR3 在日本血吸虫感染的背景下发挥了潜在作用，并且可能加速日本血吸虫相关肝脏病理的进展。