1_45dpi_No infection.fastq.gz

<i>Entamoeba (E.) histolytica</i> is a major global health concern as the causative agent of amoebic colitis, yet research is hindered by the lack of an ideal animal model. While <i>E. muris </i>has been traditionally considered non-pathogenic, our study demonstrates that it induces a colitis-like pathology in BALB/c mice, making it a promising model for studying <i>E. histolytica </i>infection. Using a fecal-oral infection route, we confirmed successful <i>E. muris</i> colonization, leading to colonic inflammation characterized by early CD4+ T-cell infiltration and FOXP3+ regulatory T-cell recruitment. We further demonstrate that T-cell immunity is essential for <i>E. muris</i> colonization, as T-cell-depleted BALB/c mice and T-cell-deficient BALB/c nude mice failed to support persistent infection. Additionally, infection disrupts epithelial homeostasis, impairing goblet cell generation, and induces significant shifts in gut microbiota composition, notably reducing beneficial Firmicutes species. Collectively, these findings demonstrate that <i>E. muris </i>infection induces inflammation and microbiota alterations, mirroring critical aspects of amoebic colitis, reinforcing its value as a model for studying <i>E. histolytica </i>pathogenesis and host–parasite interactions.