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Omics-based investigation of pathological liver injury induced by Echinococcus multilocularis infection in mice
Liangliang Chang1, Ming Li2, Yazhou Zhu1
1School of Basic Medicine, Ningxia Medical University, Yinchuan Ningxia China; Ningxia Key Laboratory of Infectious Disease Prevention and Control, Ningxia Medical University, Yinchuan Ningxia China.
Background:
Alveolar echinococcosis (AE) can cause severe liver injury and be fatal if left untreated. Currently, there are no effective therapeutic options for AE-induced liver injury. Therefore, by exploring the changes of gene proteins in mice with damaged liver, we attempted to identify the key molecules of liver damage, and provide data that will enable the development of drugs targeting hepatic AE.
Methods:
BALB/c mice were inoculated with protoscoleces via the hepatic portal vein. Three months later, B-ultrasound examination and Hematoxylin-eosin (H&E) staining were used to confirm liver damage in mice. RNA sequencing and Liquid chromatography-mass spectrometry (LC-MS) were used to screen differentially expressed molecules associated with liver damage through bioinformatics, and Quantitative Real-Time PCR (qRT-PCR) was used to verify their expression.
Results:
B-ultrasound examination showed liver lesions in the infected group, and H&E staining showed liver inflammation, fibrosis and liver necrosis. RNA sequencing and LC-MS results showed changes in the levels of more than 1000 genes and proteins, with upregulation of immune and inflammation pathways. By contrast, the downregulated genes and proteins were mostly involved in various metabolic reactions. Correlation analysis was conducted between the transcriptome data and proteome data. The results revealed 240 differentially expressed genes, of which 192 were upregulated, and 48 were downregulated. Many of these genes were involved in metabolic reactions, such as Catalase (Cat), fatty acid synthase (Fasn), and IL-16 genes, which may have relevance to liver injury. The results of qRT-PCR were consistent with those of bioinformatics analysis.
Conclusions:
The mechanisms of liver injury in mice infected with Echinococcus multilocularis are complex, involving abnormal metabolism, oxidative stress, inflammatory response, and many other factors. This study provides the data for preliminary exploration for the development of targeted therapies against AE.
Insights
Alveolar echinococcosis (AE) causes severe liver injury. This study identified key molecular changes in mouse liver damage, revealing abnormal metabolism and inflammation, paving the way for targeted AE therapies.
Area of Science:
- Parasitology
- Hepatology
- Molecular Biology
Background:
- Alveolar echinococcosis (AE) poses a significant threat, causing severe liver injury and potential fatality.
- Current therapeutic options for AE-induced liver injury are limited.
- Identifying molecular targets is crucial for developing effective treatments for hepatic AE.
Purpose of the Study:
- To investigate molecular alterations in mouse livers damaged by Echinococcus multilocularis infection.
- To identify key genes and proteins involved in AE-induced liver injury.
- To provide foundational data for the development of targeted therapies against hepatic AE.
Main Methods:
- BALB/c mice were infected with Echinococcus multilocularis protoscoleces.
- Liver damage was confirmed using B-ultrasound and Hematoxylin-eosin staining.
- RNA sequencing, LC-MS, and qRT-PCR were employed to identify and verify differentially expressed genes and proteins.
Main Results:
- Confirmed liver inflammation, fibrosis, and necrosis in infected mice.
- Identified over 1000 differentially expressed genes and proteins, with upregulated immune/inflammation pathways and downregulated metabolic pathways.
- Highlighted 240 differentially expressed genes, including Catalase (Cat), fatty acid synthase (Fasn), and IL-16, potentially linked to liver injury.
Conclusions:
- AE-induced liver injury involves complex mechanisms including abnormal metabolism, oxidative stress, and inflammation.
- This research offers crucial data for the preliminary development of targeted therapies for AE.
- Further research into identified molecular pathways can advance AE treatment strategies.
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