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Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
Published on: February 22, 2019
Understanding pathogen-host interplay by expression profiles of lncRNA and mRNA in the liver of Echinococcus
Xiaofeng Nian1,2, Li Li1, Xusheng Ma3
1State Key Laboratory of Veterinary Etiological Biology, National Professional Laboratory for Animal Echinococcosis, Key Laboratory of Veterinary Parasitology of Gansu Province, Key Laboratory of Zoonoses of Agriculture Ministry, Lanzhou Veterinary Research Institute, CAAS, Lanzhou, Gansu, P. R. China.
Abstract:
Almost all Echinococcus multilocularis (Em) infections occur in the liver of the intermediate host, causing a lethal zoonotic helminthic disease, alveolar echinococcosis (AE). However, the long non-coding RNAs (lncRNAs) expression profiles of the host and the potential regulatory function of lncRNA during Em infection are poorly understood. In this study, the profiles of lncRNAs and mRNAs in the liver of mice at different time points after Em infection were explored by microarray. Thirty-one differentially expressed mRNAs (DEMs) and 68 differentially expressed lncRNAs (DELs) were found continuously dysregulated. These DEMs were notably enriched in "antigen processing and presentation", "Th1 and Th2 cell differentiation" and "Th17 cell differentiation" pathways. The potential predicted function of DELs revealed that most DELs might influence Th17 cell differentiation and TGF-β/Smad pathway of host by trans-regulating SMAD3, STAT1, and early growth response (EGR) genes. At 30 days post-infection (dpi), up-regulated DEMs were enriched in Toll-like and RIG-I-like receptor signaling pathways, which were validated by qRT-PCR, Western blotting and downstream cytokines detection. Furthermore, flow cytometric analysis and serum levels of the corresponding cytokines confirmed the changes in cell-mediated immunity in host during Em infection that showed Th1 and Th17-type CD4+ T-cells were predominant at the early infection stage whereas Th2-type CD4+ T-cells were significantly higher at the middle/late stage. Collectively, our study revealed the potential regulatory functions of lncRNAs in modulating host Th cell subsets and provide novel clues in understanding the influence of Em infection on host innate and adaptive immune response.
Insights
This study explores long non-coding RNAs (lncRNAs) in Echinococcus multilocularis (Em) infection, revealing their role in modulating host immune responses, particularly T-helper cell differentiation, offering new insights into alveolar echinococcosis (AE).
Area of Science:
- Immunology
- Molecular Biology
- Parasitology
Background:
- Alveolar echinococcosis (AE), caused by Echinococcus multilocularis (Em), primarily affects the liver and is lethal.
- The role of long non-coding RNAs (lncRNAs) in host response to Em infection remains largely unknown.
Purpose of the Study:
- To investigate lncRNA and mRNA expression profiles in the mouse liver during Em infection.
- To elucidate the potential regulatory functions of lncRNAs in host immune modulation during AE.
Main Methods:
- Microarray analysis of lncRNA and mRNA expression in infected mouse livers at different time points.
- Bioinformatic analysis to identify differentially expressed genes (DEGs) and predict lncRNA functions.
- Validation using qRT-PCR, Western blotting, cytokine detection, and flow cytometry.
Main Results:
- Identified 68 differentially expressed lncRNAs (DELs) and 31 differentially expressed mRNAs (DEMs).
- DEMs were enriched in pathways like "antigen processing and presentation" and T-helper cell differentiation.
- DELs predicted to influence Th17 cell differentiation and TGF-β/Smad signaling by regulating SMAD3, STAT1, and EGR genes.
- Observed shifts in T-helper cell populations (Th1/Th17 early, Th2 later) and validated innate immune pathway activation.
Conclusions:
- lncRNAs play a potential regulatory role in host immune responses during Em infection.
- lncRNAs may modulate host T-helper cell subsets and innate/adaptive immunity.
- Findings provide novel insights into the host-parasite interactions in alveolar echinococcosis.
