ArticleParasites & vectors2025
Acanthamoeba castellanii cysteine protease 3 promotes M1 macrophage polarization through the TLR4/NF‑κB pathway.
Article in Parasites & vectors, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- PPAR-γ participates in macrophage polarization induced by Pentatrichomonas hominis.Medical microbiology and immunology · 2026Article
- Oxidative Stress and Redox Imbalance inInternational journal of molecular sciences · 2026Review
- M2 macrophage associated genes shape prognosis and tumor progression in human colorectal cancer.iScience · 2026Article
- Signal peptide variation in cyst lectins as a potential marker for pathogenic Acanthamoeba spp.Parasites & vectors · 2026Article
- Dual immune armies in glaucoma: microglia and monocyte-derived macrophages.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundAcanthamoeba spp., which are free-living protozoan parasites, are etiological agents for Acanthamoeba keratitis and granulomatous amoebic encephalitis. Macrophages participate in the host defense response to resist Acanthamoeba spp. This study examined the effect of Acanthamoeba castellanii cysteine protease 3 (AcCP3) on macrophage activation during inflammatory responses and explored the underlying mechanisms.
methodsThe effects of recombinant AcCP3 (rAc-CP3) stimulation on inflammatory factor levels and macrophage polarization were examined using murine macrophage cells (RAW264.7 cells). Western blotting assay was carried out for analyzing TLR4/NF‑κB pathway-related protein levels. In addition, phosphorylated NF-κB was examined for its nuclear transport using immunofluorescence. The effect of the NF-κB inhibitor pyrrolidinedithiocarbamate ammonium (PDTC) on rAc-CP3-induced M1 polarization was analyzed. Furthermore, RAW264.7 cells were co-cultivated using AcCP3 knockdown trophozoites to examine indicators of M1 polarization and pathway-related protein levels.
resultsAs revealed by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and enzyme-linked immunosorbent assays, treatment with rAc-CP3 upregulated the mRNA, protein, and secretion levels, respectively, of Il6, Il1b, Tnfa, and Ifng in macrophages. Flow cytometric analysis demonstrated that rAc-CP3 promoted Cd86
conclusionsAcCP3 promotes M1 macrophage polarization through the TLR4/NF-κB pathway and may exacerbate inflammation through upregulating pro-inflammatory cytokines.
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