ArticlePLoS pathogens2022
Gene expression of axenically-isolated clinical Entamoeba histolytica strains and its impact on disease severity of amebiasis.
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 8 papers.
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8 citing papers in PubMed, 10 citations in OpenAlex.
- Entamoeba histolytica clones presenting transient virulent phenotypes: subsequent fate of forcibly induced virulent clones by hamster's liver abscess model.Gut pathogens · 2026Article
- Entamoeba muris provides a mouse model for amoebic colitis pathology characterized by T cell associated colonization.Scientific reports · 2025Article
- Exploring virulence and stress response inMicrobiology spectrum · 2025Article
- Work with me here: variations in genome content and emerging genetic tools in Entamoeba histolytica.Trends in parasitology · 2025Review
- Genes differentially expressed between pathogenic and non-pathogenic Entamoeba histolytica clones influence pathogenicity-associated phenotypes by multiple mechanisms.PLoS pathogens · 2023Article
- Diversity and Plasticity of Virulent Characteristics ofTropical medicine and infectious disease · 2023Review
- Attenuation of In Vitro and In Vivo Virulence Is Associated with Repression of Gene Expression of AIG1 Gene inPathogens (Basel, Switzerland) · 2023Article
- The evolutionary cancer genome theory and its reasoning.Genetics in medicine open · 2023Review
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The severity of Entamoeba histolytica infection is determined by host immunology, pathogen virulence, and the intestinal environment. Conventional research for assessing pathogen virulence has been mainly performed using laboratory strains, such as a virulent HM-1: IMSS (HM-1) and an avirulent Rahman, under various artificial environmental conditions because of the difficulties of axenic isolation of the clinical strains. However, it is still unclear whether scientific knowledge based on laboratory strains are universally applicable to the true pathogenesis. Hereby, we performed transcriptomic analysis of clinical strains from patients with different degrees of disease severity, as well as HM-1 under different conditions. Even after several months of axenization, Clinical strains show the distinct profile in gene expression during in vitro passage, moreover, difference between any 2 of these strains was much greater than the changes on the liver challenge. Interestingly, 26 DEGs, which were closely related to the biological functions, were oppositely up- or down regulated between virulent Ax 19 (liver abscess) and avirulent Ax 11 (asymptomatic carrier). Additionally, RNAseq using laboratory strain (HM1) showed more than half of genes were differently expressed between continuously in vitro passaged HM1 (in vitro HM1) and periodically liver passaged HM1 (virulent HM1), which was much greater than the changes on the liver passage of virulent HM1. Also, transcriptomic analysis of a laboratory strain revealed that continuous environmental stress enhances its virulence via a shift in its gene expression profile. Changes in gene expression patterns on liver abscess formation were not consistent between clinical and laboratory strains.
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