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Abstract
Fasciola gigantica produces excretory-secretory products (ESPs) with immune-modulating effects to promote its own survival. In this study, we performed RNA-seq to gain a comprehensive global understanding of changes in the expression of mRNAs, miRNAs, lncRNAs, and circRNAs in goat peripheral blood mononuclear cells (PBMCs) treated with F. gigantica ESPs. A total of 1,544 differently expressed mRNAs (790 upregulated and 754 downregulated genes), 30 differently expressed miRNAs (24 upregulated and 6 downregulated genes), 136 differently expressed circRNAs (83 upregulated and 53 downregulated genes), and 1,194 differently expressed lncRNAs (215 upregulated and 979 downregulated genes) were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that F. gigantica ESPs altered the expression of genes associated with the host immune response, receptor signaling, disease and metabolism. Results from RNA-seq were validated by qRT-PCR. These findings provide an important resource for future investigation of the role of mRNAs and non-coding RNAs in mediating the immune-modulating effects of F. gigantica ESPs.
Highlights
Fasciolosis, caused by Fasciola gigantica and F. hepatica, is a significant parasitic disease, causing huge economic losses to livestock and serious adverse impact on public health [1,2,3]
By using co-immunoprecipitation coupled with tandem mass spectrometry, we identified 14, 16, 9, and 9 proteins in F. hepatica excretory-secretory products (ESPs) (FhESPs) that can bind to cytokines IL2, IL17, IFN-g, and goat peripheral blood mononuclear cells (PBMCs) [9]
We performed global RNA-seq to profile the expression of messenger RNAs (mRNAs), miRNAs, lncRNAs, and circRNAs in goat PBMCs exposed to F. gigantica ESPs
Summary
Fasciolosis, caused by Fasciola gigantica and F. hepatica, is a significant parasitic disease, causing huge economic losses to livestock and serious adverse impact on public health [1,2,3]. The annual global economic losses to livestock production caused by liver fluke infection exceed $3 billion [6]. Exploring the molecular mechanisms of interaction between the host and liver flukes would enhance our understanding of the host immune response and assist in identifying potential targets for the development of therapeutic interventions against fasciolosis. Liver flukes employ a raft of strategies to subvert the host’s immune response, including the secretion of excretory-secretory products (ESPs) to modulate the host’s immune responses, to facilitate their own survival and to establish long-term infection [7, 8]. A proteomic analysis of FgESPs interacting with buffalo serum at different infection periods (42, 70, and 98 dpi) identified 18 proteins after F. gigantica infection, including 13 cathepsin proteins, 4 glutathione S-transferase proteins, and 1 calcium-binding protein [10]
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