Department of Human Parasitology, Guilin Medical University, Guilin, 541199, Guangxi Zhuang, China.
Department of Immunology, Faculty of Medicine, Qinghai University, Xining, 810001, Qinghai, China.
Parasit Vectors. 2021 Dec 2;14(1):593. doi: 10.1186/s13071-021-05037-1.
Echinococcus multilocularis is the causative agent of human hepatic alveolar echinococcosis (AE). AE can cause damage to several organs, primarily the liver, and have severe outcomes, such as hepatic failure and encephalopathy. The main purpose of this study was to explore the interactions between hepatic stellate cells (HSCs) and E. multilocularis protoscoleces (PSCs). The results of this study provide an experimental basis for further examination of the pathogenesis of hepatic fibrosis due to AE infection.
We investigated the role of Echinococcus multilocularis (Echinococcus genus) PSCs in hepatic fibrosis by examining structural changes and measuring hepatic fibrosis-related protein levels in cocultures of PSCs and human HSCs. Structural changes were detected by transmission electron microscopy (TEM), and levels of the hepatic fibrosis-related proteins collagen I (Col-I), alpha-smooth muscle actin (α-SMA) and osteopontin (OPN) were measured by western blotting and enzyme-linked immunosorbent assay (ELISA).
Under coculture (1) both PSCs and HSCs exhibited morphological changes, as observed by TEM; (2) Col-I, α-SMA, and OPN expression levels, which were determined by western blotting and ELISA, significantly increased after 3 days of incubation.
The results of this study provide insights into the molecular mechanisms of AE-induced hepatic fibrosis.
多房棘球绦虫是人体泡型包虫病(AE)的病原体。AE 可导致多个器官受损,主要是肝脏,并导致严重后果,如肝衰竭和脑病。本研究的主要目的是探讨肝星状细胞(HSCs)与多房棘球蚴原头节(PSCs)之间的相互作用。本研究的结果为进一步研究 AE 感染引起的肝纤维化发病机制提供了实验依据。
通过观察 PSCs 和人 HSCs 共培养物中的结构变化和测量肝纤维化相关蛋白水平,研究多房棘球绦虫(棘球属)PSCs 在肝纤维化中的作用。通过透射电子显微镜(TEM)检测结构变化,通过 Western blot 和酶联免疫吸附试验(ELISA)测量肝纤维化相关蛋白胶原 I(Col-I)、α-平滑肌肌动蛋白(α-SMA)和骨桥蛋白(OPN)的水平。
共培养(1)PSCs 和 HSCs 均发生形态学变化,TEM 观察到;(2)孵育 3 天后,Western blot 和 ELISA 测定 Col-I、α-SMA 和 OPN 的表达水平显著增加。
本研究结果为了解 AE 诱导的肝纤维化的分子机制提供了线索。