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Table_1_Roles of TLR7 in Schistosoma japonicum Infection-Induced Hepatic Pathological Changes in C57BL/6 Mice.xlsx

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https://figshare.com/articles/dataset/Table_1_Roles_of_TLR7_in_Schistosoma_japonicum_Infection-Induced_Hepatic_Pathological_Changes_in_C57BL_6_Mice_xlsx/16768591
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S. japonicum infection can induce granulomatous inflammation in the liver of the host. Granulomatous inflammation limits the spread of infection and plays a role in host protection. Toll-like receptor 7 (TLR7) is an endosomal TLR that recognizes single-stranded RNA (ssRNA). In this study, the role of TLR7 in S. japonicum infection-induced hepatitis was investigated in both normal and TLR7 knockout (KO) C57BL/6 mice. The results indicated that TLR7 KO could aggravate S. japonicum infection-induced damage in the body, with less granuloma formation in the tissue, lower WBCs in blood, and decreased ALT and AST in the serum. Then, the expression of TLR7 was detected in isolated hepatic lymphocytes. The results indicated that the percentage of TLR7+ cells was increased in the infected mice. Hepatic macrophages, DCs, and B cells could express TLR7, and most of the TLR7-expressing cells in the liver of infected mice were macrophages. The percentage of TLR7-expressing macrophages was also increased after infection. Moreover, macrophages, T cells, and B cells showed significant changes in the counts, activation-associated molecule expression, and cytokine secretion between S. japonicum-infected WT and TLR7 KO mice. Altogether, this study indicated that TLR7 could delay the progression of S. japonicum infection-induced hepatitis mainly through macrophages. DCs, B cells, and T cells were involved in the TLR7-mediated immune response.

日本血吸虫(S. japonicum)感染可诱发宿主肝脏出现肉芽肿性炎症。该炎症可限制感染扩散,并在宿主防御过程中发挥作用。Toll样受体7(TLR7)是一类识别单链RNA(ssRNA)的内体Toll样受体。本研究以野生型(WT)及TLR7敲除(KO)C57BL/6小鼠为模型,探究了TLR7在日本血吸虫感染诱发肝炎中的作用。结果显示,TLR7敲除可加重日本血吸虫感染所致的机体损伤,具体表现为组织内肉芽肿形成减少、血液白细胞计数降低,以及血清丙氨酸氨基转移酶(ALT)与天冬氨酸氨基转移酶(AST)水平下降。研究人员对分离获得的肝脏淋巴细胞中TLR7的表达情况进行了检测,结果发现感染小鼠体内TLR7阳性细胞的占比升高。肝脏巨噬细胞、树突状细胞(DCs)及B细胞均可表达TLR7,而感染小鼠肝脏内多数表达TLR7的细胞为巨噬细胞;感染后,表达TLR7的巨噬细胞占比同样有所升高。此外,与感染的野生型小鼠相比,TLR7敲除感染小鼠的巨噬细胞、T细胞及B细胞在细胞数量、活化相关分子表达及细胞因子分泌方面均出现显著变化。综上,本研究表明TLR7主要通过巨噬细胞延缓日本血吸虫感染诱发肝炎的进程,树突状细胞、B细胞及T细胞亦参与了TLR7介导的免疫应答。
创建时间:
2021-10-08
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