Hydatid cyst fluid promotes peri-cystic fibrosis in cystic echinococcosis by suppressing miR-19 expression

Background: echinococcus granulosus infection causes cystic echinococcosis (ce); the generation of liver fibrosis around the parasitic larval cyst (metacestode) may play a major role in the spontaneous limitation of the parasitic growth; however,fibrogenesis has received little attention in ce. it has been reported that mir-19b plays a role in various diseases,including infectious diseases,by regulating fibrogenesis. however,its function in the development of liver fibrosis in e. granulosus infection is unknown. methods: the expression of mir-19b and genes that are involved in liver fibrosis were analysed in e. granulosus-infected human livers using qrt-pcr. the role of mir-19b on hepatic stellate cells (lx-2 cells in vitro) treated with hydatid cyst fluid (hcf) was then analysed by 3-(4,5-dimet-hylthiazol-2-yl)-2,4-diphenyl-tetrazolium bromide (mtt) assay,qrt-pcr,western blot and flow cytometry. results: the results showed that the expression of mir-19 was significantly reduced in the pericystic collagen-rich liver tissue of ce patients,compared to normal liver. incubation of lx-2 cells (in vitro) with hcf induced a decreased proliferation of these cells and a reduced expression of mir-19,inversely correlated with the expression of collagen 1a1 and tgf-β receptor ii (tβrii). conversely,overexpression of mir-19 by lx-2 cells inhibited the proliferation of these cells and led to decreased tβrii expression. conclusions: our study provides new evidence for the intervention of mirnas in the regulation of fibrosis in infectious diseases; it suggests that e. granulosus can inhibit mir-19 liver expression and promote fibrosis through the increase in tβrii,the activation of hepatic stellate cells and extracellular matrix production. © 2016 zhang et al.