Background Alveolar echinococcosis (AE) is caused by parasitic infection by Echinococcus multilocularis. Its diagnosis is usually based on clinical symptoms, ultrasound, and other imaging methods. MicroRNAs (miRNAs) play important roles in disease processes and can exist in a highly stable cell-free form in body fluids. It is important to identify specific, sensitive diagnostic markers for early diagnosis and evaluation of AE. In this study, we examined hsa-miR-125b-5p as a potential plasma biomarker of E. multilocularis infection. Methods Plasma samples from patients with AE and healthy individuals were screened for the presence of five miRNAs using miRNA chips. We used quantitative polymerase chain reaction to measure miRNA expression levels in plasma and liver tissue samples from patients with AE. Results hsa-miR-125b-5p was stably upregulated in the plasma and liver tissue samples from patients with AE. Conclusions The results suggest that hsa-miR-125b-5p may be a promising biomarker for early, non-invasive diagnosis of AE.
There are two main types of echinococcosis, namely alveolar echinococcosis (AE) and cystic echinococcosis (CE). They are zoonotic parasitic diseases caused by the metacestodes of Echinococcus multilocularis and Echinococcus granulosus. In order to explore the gut microbiome composition of patients with echinococcosis, we analyzed fecal samples of seven patients with AE, six patients with CE, and 13 healthy individuals from the Qinghai-Tibetan Plateau, China. Using metagenomic next-generation sequencing, we identified fecal bacteria in the patients with AE and CE. The gut microbiota was analyzed by next-generation metagenomic sequencing (mNGS) to compare patients with either AE or CE against healthy individuals. We found there were some differences between them in abundant bacteria. Our results led to five findings: (1) Between patients with echinococcosis and healthy individuals, the differential bacteria were from four phyla: Firmicutes, Proteobacteria, Bacteroidetes, Actinobacteria. (2) Rothia mucilaginosa, Veillonella dispar, Veillonella atypica, Streptococcus parasanguinis, Streptococcus salivarius, and Alistipes finegoldii were abundant in the feces of patients with AE. (3) Bacteroides dorei, Parabacteroides distasonis, Escherichia sp_E4742, and Methanobrevibacter smithii were abundant in the feces of the patients with CE. (4) At the phylum and class level, compared to the AE group, the healthy group was characterized by higher numbers of Actinobacteria. (5) At the family level, Lachnospiraceae and Eubacteriaceae were more abundant in the feces of healthy individuals than in AE patients. The genera Coprococcus, Eubacterium, and Bilophia were more abundant in the healthy group, while the genus Rothia was more abundant in the AE group. The results of this study enrich our understanding of the gut microbiome composition of patients with AE and CE in the Qinghai-Tibetan Plateau.
Background: Alveolar echinococcosis is an infectious zoonotic disease caused by Echinococcus multilocularis that is endemic to the vast pastoral areas of southern Qinghai province of China. Alveolar echinococcosis affects the human liver, and its clinical manifestations are similar to those of liver tumors. It is also called “worm cancer,” as it induces irreversible liver fibrosis and brain metastases. Alveolar echinococcosis is a serious threat to human health and is a burden to patients and economies. When detected and treated early, patients with alveolar echinococcosis have a strong chance of recovery. Therefore, it is imperative to identify early diagnostic biomarkers of the disease. MicroRNAs (miRNAs) are short, single-stranded, non-coding RNA molecules that play key roles in a wide range of biological processes, and have been recently implicated in tumorigenesis. However, little is known about the role of miRNAs in alveolar echinococcosis. We have previously reported differentially expressed miRNAs in the plasma of patients with alveolar echinococcosis and healthy individuals, using microarray assay chips. Methods: We screened 10 differentially expressed miRNAs based on their fold change and the available literature. Additionally, quantitative polymerase chain reaction was used to verify their expression in the plasma of alveolar echinococcosis patients. We found that hsa-miR-125b-5p was upregulated in the plasma and the hepatic tissue samples of alveolar echinococcosis patients; therefore, its role as a diagnostic biomarker for alveolar echinococcosis was investigated. Accordingly, hsa-miR-125b-5p was upregulated in plasma and hepatic tissue samples obtained from alveolar echinococcosis patients. Receiver operating characteristic curves showed that hsa-miR-125b-5p was associated with an area under the curve of 99.8% and 98.9% in the plasma and hepatic tissues of alveolar echinococcosis patients, respectively. Transfection of an LV-hsa-miR-125b-5p-inhibitor reduced apoptosis of L-O2 hepatocytes in vitro (P < 0.05). Thus, hsa-miR-125b-5p may promote liver cell proliferation and inhibit liver cell apoptosis.Conclusions: Taken together, hsa-miR-125b-5p may be a promising diagnostic biomarker for the early non-invasive diagnosis of alveolar echinococcosis. We plan to validate the expression of hsa-miR-125b-5p in the plasma of patients with cystic echinococcosis, alveolar echinococcosis, and other liver diseases to determine the potential of hsa-miR-125-5p as a differential biomarker in future studies.
Background Chronic infection with Clonorchis sinensis can cause hepatobiliary fibrosis and even lead to hepatobiliary carcinoma. Epstein-Barr virus-induced gene 3 protein (EBI3) is a subunit of interleukin 35, which can regulate inflammatory response and the occurrence of fibrotic diseases. Previous studies have reported that the expression of EBI3 in the serum of patients with liver cirrhosis is reduced. The present study aims to investigate the biological effects of EBI3 on liver fibrosis caused by C. sinensis and the underlying molecular mechanisms. Methods We first established a mouse model of liver fibrosis induced by C. sinensis infection and then measured the serum expression of EBI3 during the inflammatory and fibrotic phase. GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analyses were performed to investigate the potential role of EBI3 in liver fibrosis by regulating the extracellular matrix structural constituent and collagen catabolic process. Recombinant protein EBI3 (rEBI3) was added to hepatic stellate cells (HSCs) in vitro with C. sinensis antigen to explore its function. Finally, the therapeutic effect of rEBI3 was verified by intravenous injection into C. sinensis-infected mice. Results The results showed that the serum expression of EBI3 increased in the inflammatory response phase but decreased in the fibrotic phase. The excretory-secretory products of C. sinensis (Cs.ESP) were able to stimulate HSC activation, while rEBI3 reduced the activation of HSCs induced by Cs.ESP. Also, the protein expression of gp130 and downstream protein expressions of JAK1, p-JAK1, STAT3 and p-STAT3 in HSCs were increased after rEBI3 incubation. Finally, intravenously injected rEBI3 inhibited hepatic epithelial-mesenchymal transition in C. sinensis-infected mice by inhibiting HSC activation and reducing liver injury. Conclusion This study confirms that rEBI3 can attenuate C. sinensis-induced liver fibrosis by inhibiting HSC activation and may be one of the potential treatments for liver fibrosis. Graphical Abstract
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