ArticleParasitology research2019
Cytokine production and signalling in human THP-1 macrophages is dependent on Toxocara canis glycans.
Article in Parasitology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
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- Editorial: "You shall not pass" or "Let`s make a deal" - crosstalk between helminths and the host immune system.Frontiers in cellular and infection microbiology · 2023Article
- The non-glycosylated protein of Toxocara canis MUC-1 interacts with proteins of murine macrophages.PLoS neglected tropical diseases · 2022Article
- The Role of Nuclear Factor Kappa B (NF-κB) in the Immune Response against Parasites.Pathogens (Basel, Switzerland) · 2022Review
- Identification ofPathogens (Basel, Switzerland) · 2021Article
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- Regulation of human THP-1 macrophage polarization by Trichinella spiralis.Parasitology research · 2021Article
- The Two Faces of Nematode Infection: Virulence and Immunomodulatory Molecules From Nematode Parasites of Mammals, Insects and Plants.Frontiers in microbiology · 2020Review
- MGL1 Receptor Plays a Key Role in the Control ofCells · 2020Article
- LPS Inhibits Fatty Acid Absorption in Enterocytes through TNF-α Secreted by Macrophages.Cells · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of Toxocara canis antigens on cytokine production by human THP-1 macrophages was studied in vitro. Toxocara Excretory-Secretory products (TES) and recombinant mucins (Tc-MUC-2, Tc-MUC-3, Tc-MUC-4, and Tc-MUC-5) as well as deglycosylated forms of these antigens were used in the study. TES products stimulated macrophages to produce the innate proinflammatory IL-1β, IL-6, and TNF-α cytokines regardless of the presence of glycans. Recombinant mucins induced glycan-dependent cytokine production. Sugar moieties led to at least 3-fold higher production of regulatory IL-10 as well as proinflammatory cytokines. The presence of glycans on mucins also affected the downstream signalling pathways in stimulated cells. The most prominent difference was noted in AKT and AMPK kinase activation. AKT phosphorylation was observed in cells stimulated with glycosylated mucins, whereas treatment with deglycosylated antigens led to AMPK phosphorylation. MAP kinase family members such as JNK and p38 and c-Jun transcription factor were phosphorylated in both cases what suggests that toll-like receptor signalling may be involved in mucin-treated macrophages. This pathway is however modified by other signalling molecules as only mucins containing intact sugars significantly induced the production of cytokines.
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