1. Entamoeba moshkovskii as a potential model organism for Gal/GalNAc lectin intermediate subunit exhibition and functional identification.
- Author
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Li Q, Feng M, Zhang H, Zhou H, and Cheng X
- Subjects
- Phagocytosis, Lectins metabolism, Lectins genetics, Humans, Animals, Transfection, Virulence genetics, Entamoebiasis parasitology, Mice, Entamoeba genetics, Entamoeba pathogenicity, Protozoan Proteins genetics, Protozoan Proteins metabolism, Entamoeba histolytica genetics, Entamoeba histolytica pathogenicity, Entamoeba histolytica metabolism, Trophozoites metabolism
- Abstract
In humans, Entamoeba histolytica is the main pathogen causing various amoebiases, while E. moshkovskii falls between being a pathogen and non-pathogen. The two species have similar behavior patterns but differ significantly in pathogenicity, with previous studies and clinical data indicating that E. moshkovskii has a low level of pathogenicity. Meaningfully, the biological characteristics of E. moshkovskii make it a potential model organism and a protein display platform for studying the functions of important Entamoeba proteins. Here, an Amoeba-pcDNA3.1 vector capable of overexpressing E. histolytica-sourced Igl-C protein was constructed and successfully transfected into E. moshkovskii. High levels of expression of the Igl-C, EGFP, and NeoR genes were identified in Igl-C-transfected trophozoites using qRT-PCR, and they were subsequently confirmed using immunoblotting. Transfection of Igl-C protein improved the adherence and phagocytosis of E. moshkovskii, demonstrating that E. histolytica Igl mediated amoebic adhesion. Moreover, as a manifestation of protein virulence, the ability of post-transfected trophozoites to induce inflammation in host macrophages was also enhanced. In conclusion, this study utilizing the characteristics of E. moshkovskii confirmed its potential to serve as a model organism. E. moshkovskii could replace E. histolytica as the target of gene editing, allowing more efficient study of amoebic pathogenicity.
- Published
- 2024
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