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<p><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.</p>

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Entamoeba muris provides a mouse model for amoebic colitis pathology characterized by T cell associated colonization

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月14日

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  • Tae Hun Ha,
  • Sang Hyeok Seok,
  • Heok won An,
  • Jong-Wan Kwon,
  • Gyeong Min Yoon,
  • Yu Jin Lee,
  • Na Yun Lee,
  • Hyeon Ah Kim,
  • Won Gi Yoo,
  • Su-Hyung Lee,
  • Jun Won Park

摘要

Entamoeba (E.) histolytica 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 E. muris 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 E. histolytica infection. Using a fecal-oral infection route, we confirmed successful E. muris 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 E. muris 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 E. muris infection induces inflammation and microbiota alterations, mirroring critical aspects of amoebic colitis, reinforcing its value as a model for studying E. histolytica pathogenesis and host–parasite interactions.