ArticleParasites & vectors2017
Clonorchis sinensis lysophospholipase A upregulates IL-25 expression in macrophages as a potential pathway to liver fibrosis.
Article in Parasites & vectors, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Hepatic ferroptosis induced by Clonorchis sinensis exacerbates liver fibrosis.PLoS neglected tropical diseases · 2025Article
- A dysregulated sebum-microbial metabolite-IL-33 axis initiates skin inflammation in atopic dermatitis.The Journal of experimental medicine · 2022Article
- Exploring the role of macrophages in determining the pathogenesis of liver fluke infection.Parasitology · 2022Review
- Article
- Novel mechanism of hepatobiliary system damage and immunoglobulin G4 elevation caused byWorld journal of clinical cases · 2021Review
- Circular RNA circUbe2k promotes hepatic fibrosis via sponging miR-149-5p/TGF-β2 axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Risk Factors forFrontiers in public health · 2021Article
- In vivo and in vitro studies using Clonorchis sinensis adult-derived total protein (CsTP) on cellular function and inflammatory effect in mouse and cell model.Parasitology research · 2020Article
- Focus on the glycerophosphocholine pathway in choline phospholipid metabolism of cancer.NMR in biomedicine · 2019Review
- The MAPK Signaling Pathways as a Novel Way in Regulation and Treatment of Parasitic Diseases.Diseases (Basel, Switzerland) · 2019Review
- The Role of Stroma in Cholangiocarcinoma: The Intriguing Interplay between Fibroblastic Component, Immune Cell Subsets and Tumor Epithelium.International journal of molecular sciences · 2018Review
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Authors and funding
11 authors.
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Abstract
backgroundLiver fibrosis is an excessive wound-healing reaction that requires the participation of inflammatory cells and hepatic stellate cells (HSCs). The pathogenesis of liver fibrosis caused by viruses and alcohol has been well characterized, but the molecular mechanisms underlying liver fibrosis induced by the liver fluke Clonorchis sinensis are poorly understood. Lysophospholipase A (LysoPLA), which deacylates lysophospholipids, plays a critical role in mediating the virulence and pathogenesis of parasites and fungi; however, the roles of C. sinensis lysophospholipase A (CsLysoPLA) in C. sinensis-induced liver fibrosis remain unknown.
methodsA mouse macrophage cell line (RAW264.7) was cultured and treated with CsLysoPLA. IL-25 and members of its associated signaling pathway were detected by performing quantitative real-time PCR, Western blotting and immunofluorescent staining. A human hepatic stellate cell line (LX-2) was cultured and exposed to IL-25. LX-2 cell activation markers were examined via quantitative real-time PCR, Western blotting and immunofluorescent staining. Migration was analyzed in transwell plates.
resultsTreating RAW264.7 cells with CsLysoPLA significantly induced IL-25 expression. Elevated PKA, B-Raf, and ERK1/2 mRNA levels and phosphorylated B-Raf and ERK1/2 were detected in CsLysoPLA-stimulated RAW264.7 cells. The PKA inhibitor H-89 weakened B-Raf and ERK1/2 phosphorylation whereas the AKT activator SC79 attenuated ERK1/2 phosphorylation in RAW264.7 cells. Both H-89 and SC79 inhibited CsLysoPLA-induced IL-25 upregulation. In addition, stimulation of LX-2 cells with IL-25 upregulated the expression of mesenchymal cell markers, including α-smooth muscle actin (α-SMA) and collagen type I (Collagen-I), and promoted cell migration.
conclusionsCsLysoPLA activates HSCs by upregulating IL-25 in macrophages through the PKA-dependent B-Raf/ERK1/2 pathway and potentially promotes hepatic fibrosis during C. sinensis infection.
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