Jiang Tingting, Wu Xiaoying, Zhou Hao, Hu Yuan, Cao Jianping
National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention, (Chinese Center for Tropical Diseases Research), Key Laboratory of Parasite and Vector Biology, National Health Commission of People's Republic of China, World Health Organization Collaborating Center for Tropical Diseases, Shanghai 200025, China.
The School of Global Health, Chinese Center for Tropical Diseases Research, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Trop Med Infect Dis. 2023 Feb 17;8(2):124. doi: 10.3390/tropicalmed8020124.
Schistosomiasis japonica is a zoonotic parasitic disease causing liver fibrosis. Liver sinusoidal endothelial cells (LSECs) exhibit fenestrations, which promote hepatocyte regeneration and reverses the process of liver fibrosis. To investigate the pathological changes of LSECs in schistosomiasis, we established a Schistosomiasis model. The population, phenotype, and secretory function of LSECs were detected by flow cytometry at 20, 28, and 42 days post infection. The changes in LSEC fenestration and basement membrane were observed through scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Quantitative real-time PCR and Western blotting were used to detect the expression of molecules associated with epithelial-mesenchymal transition (EMT) and fibrosis of LSECs and the liver. The flow cytometry results showed that the total LSEC proportions, differentiated LSEC proportions, and nitric oxide (NO) secretion of LSECs were decreased, and the proportion of dedifferentiated LSECs increased significantly post infection. The electron microscopy results showed that the number of fenestrate was decreased and there was complete basement membrane formation in LSECs following infection. The qPCR and Western blot results showed that EMT, and fibrosis-related indicators of LSECs and the liver changed significantly during the early stages of infection and were aggravated in the middle and late stages. The pathological changes in LSECs may promote EMT and liver fibrosis induced by infection.
日本血吸虫病是一种导致肝纤维化的人畜共患寄生虫病。肝窦内皮细胞（LSECs）有窗孔，可促进肝细胞再生并逆转肝纤维化进程。为研究日本血吸虫病中LSECs的病理变化，我们建立了血吸虫病模型。在感染后20、28和42天，通过流式细胞术检测LSECs的数量、表型和分泌功能。通过扫描电子显微镜（SEM）和透射电子显微镜（TEM）观察LSEC窗孔和基底膜的变化。采用定量实时PCR和蛋白质印迹法检测与LSECs和肝脏上皮-间质转化（EMT）及纤维化相关分子的表达。流式细胞术结果显示，感染后LSECs的总比例、分化LSECs比例和一氧化氮（NO）分泌减少，去分化LSECs比例显著增加。电子显微镜结果显示，感染后LSECs的窗孔数量减少，且形成了完整的基底膜。qPCR和蛋白质印迹结果显示，感染早期LSECs和肝脏的EMT及纤维化相关指标发生显著变化，在感染中晚期加重。LSECs的病理变化可能促进感染诱导的EMT和肝纤维化。
