ArticlePLoS pathogens2022
Fasciola hepatica is refractory to complement killing by preventing attachment of mannose binding lectin (MBL) and inhibiting MBL-associated serine proteases (MASPs) with serpins.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- In vitro Host-Parasite Models Combined With Proteomics Reveal Cell Type-Specific Responses of Early Migrating Fasciola hepatica Juveniles.Molecular & cellular proteomics : MCP · 2026Article
- Fibrinolysis-unrelated functions of the plasminogen/plasmin system: A gateway to successful parasitism?Current research in parasitology & vector-borne diseases · 2026Review
- Early host-parasite interaction models reveal a key role for fibrinolysis in Fasciola hepatica intestinal migration.Parasites & vectors · 2025Article
- Deciphering theBiomolecules · 2025Review
- Article
- Binding and cleavage of pro-urokinase by a tegument extract of Fasciola hepatica newly excysted juveniles activate the host fibrinolytic system.Veterinary research · 2025Article
- Moonlighting on the Fasciola hepatica tegument: Enolase, a glycolytic enzyme, interacts with the extracellular matrix and fibrinolytic system of the host.PLoS neglected tropical diseases · 2024Article
- An Update on the Pathogenesis of Fascioliasis: What Do We Know?Research and reports in tropical medicine · 2024Review
- Glycan Complexity and Heterogeneity of Glycoproteins in Somatic Extracts and Secretome of the Infective Stage of the Helminth Fasciola hepatica.Molecular & cellular proteomics : MCP · 2023Article
- Molecular Characterization of the Interplay betweenInternational journal of molecular sciences · 2023Article
- Hidden in plain sight: How helminths manage to thrive in host blood.Frontiers in parasitology · 2023Review
- Fasciolosis: pathogenesis, host-parasite interactions, and implication in vaccine development.Frontiers in veterinary science · 2023Review
- Article
- Proteomics coupled with in vitro model to study the early crosstalk occurring between newly excysted juveniles of Fasciola hepatica and host intestinal cells.PLoS neglected tropical diseases · 2022Article
- Knockout of liver fluke granulin, Ov-grn-1, impedes malignant transformation during chronic infection with Opisthorchis viverrini.PLoS pathogens · 2022Article
- Immunomodulators secreted from parasitic helminths act on pattern recognition receptors.Frontiers in parasitology · 2022Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system is a first-line innate host immune defence against invading pathogens. It is activated via three pathways, termed Classical, Lectin and Alternative, which are mediated by antibodies, carbohydrate arrays or microbial liposaccharides, respectively. The three complement pathways converge in the formation of C3-convertase followed by the assembly of a lethal pore-like structure, the membrane attack complex (MAC), on the pathogen surface. We found that the infectious stage of the helminth parasite Fasciola hepatica, the newly excysted juvenile (NEJ), is resistant to the damaging effects of complement. Despite being coated with mannosylated proteins, the main initiator of the Lectin pathway, the mannose binding lectin (MBL), does not bind to the surface of live NEJ. In addition, we found that recombinantly expressed serine protease inhibitors secreted by NEJ (rFhSrp1 and rFhSrp2) selectively prevent activation of the complement via the Lectin pathway. Our experiments demonstrate that rFhSrp1 and rFhSrp2 inhibit native and recombinant MBL-associated serine proteases (MASPs), impairing the primary step that mediates C3b and C4b deposition on the NEJ surface. Indeed, immunofluorescence studies show that MBL, C3b, C4b or MAC are not deposited on the surface of NEJ incubated in normal human serum. Taken together, our findings uncover new means by which a helminth parasite prevents the activation of the Lectin complement pathway to become refractory to killing via this host response, in spite of presenting an assortment of glycans on their surface.
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