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Purpose <p>Alveolar echinococcosis (AE), a zoonotic parasitic disease caused by the larval metacestode of <i>Echinococcus multilocularis</i> (<i>E. multilocularis</i>), primarily affects the liver and can invide other organs. Given its extremely poor prognsis, witha 10-year mortality rate exceeding 90% in untreated cases, this study aimed to investigate the characteristics and compositional alterations of the intestinal microbiota in AE-infected hosts and evaluate associated intestinal mucosal damage.</p> Methods <p>We established a mouse model of AE for analysis. Fecal samples were collected from 12 AE-infected mice and 12 age-matched healthy controls at 3 and 6 months post-infection. Gut microbiota composition was assessed by 16S rRNA gene sequencing. Intestinal tissues were subjected to histopathological exnamination using hematoxylin-eosin staining (H&amp;E staining), Alcian blue-glucogen staining (AB-PAS staining), and Lendrum’s fluorescent peach red staining, to evaluate mucosal structural integrity and quantify the Paneth and goblet cells.</p> Results <p>The analysis revealed significant alterations in intestinal microbiota diversity and composition in AE-infected mice compared with controls, with changes becoming more pronounced as the infection progressed. Minimal disruption in microbial ecology was observed at 3&#xa0;months, whereas substantial reductions in alpha diversity and distinct shifts in beta diversity emerged after 6&#xa0;months of chronic infection. Phylum-level analysis showed an early increase in Verrucomicrobiota, Bacteroidota, and Campylobacterota at 3&#xa0;months, followed by a marked enrichment of Verrucomicrobiota and Actinobacteriota at 6&#xa0;months when compared with controls. At the genus level, AE infection led to a rapid depletion of <i>Ligilactobacillus</i> and <i>Lactobacillus</i> between 3 and 6&#xa0;months, while <i>Akkermansia</i> abundance significantly increased. Histopathological examination of intestinal tissue further demonstrated severe mucosal damage, including villous atrophy, reduced crypt depth, a pronounced decrease in Paneth cell density (<i>P</i> &lt; 0.01), and reduced goblet cell counts (<i>P</i> &lt; 0.05), collectively indicating compromised intestinal barrier integrity.</p> Conclusion <p>AE infection induces progressive gut microbiota dysbiosis and compromises intestinal barrier integrity. The specific microbial shifts, particularly the depletion of <i>Ligilactobacillus</i> and enrichment of <i>Akkermansia</i>, represent promising diagnostic biomarkers and potential targets for probiotic supplementation or microbial modulation. To further clarify their roles, future research should incorporate multi-omics strategies, including metagenomics and metabolomics, within larger cohorts to better characterize microbiota-host metabolic interactions and to validate stage-specific microbial biomarkers in AE.</p>

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Investigation of the Alterations in the Gut Microbiota and Intestinal Mucosa in Mice Infected with Echinococcus multilocularis

  • 期刊论文

  • 发表日期：

    2025年11月14日

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  • Deping Cao,
  • Wenjun Huang,
  • Mingquan Pang,
  • Jiajing Li,
  • Haitao Huang,
  • Hui Ma,
  • Dayu Li,
  • Yufei Qin,
  • Xiaohong Peng,
  • Haining Fan

摘要

Purpose

Alveolar echinococcosis (AE), a zoonotic parasitic disease caused by the larval metacestode of Echinococcus multilocularis (E. multilocularis), primarily affects the liver and can invide other organs. Given its extremely poor prognsis, witha 10-year mortality rate exceeding 90% in untreated cases, this study aimed to investigate the characteristics and compositional alterations of the intestinal microbiota in AE-infected hosts and evaluate associated intestinal mucosal damage.

Methods

We established a mouse model of AE for analysis. Fecal samples were collected from 12 AE-infected mice and 12 age-matched healthy controls at 3 and 6 months post-infection. Gut microbiota composition was assessed by 16S rRNA gene sequencing. Intestinal tissues were subjected to histopathological exnamination using hematoxylin-eosin staining (H&E staining), Alcian blue-glucogen staining (AB-PAS staining), and Lendrum’s fluorescent peach red staining, to evaluate mucosal structural integrity and quantify the Paneth and goblet cells.

Results

The analysis revealed significant alterations in intestinal microbiota diversity and composition in AE-infected mice compared with controls, with changes becoming more pronounced as the infection progressed. Minimal disruption in microbial ecology was observed at 3 months, whereas substantial reductions in alpha diversity and distinct shifts in beta diversity emerged after 6 months of chronic infection. Phylum-level analysis showed an early increase in Verrucomicrobiota, Bacteroidota, and Campylobacterota at 3 months, followed by a marked enrichment of Verrucomicrobiota and Actinobacteriota at 6 months when compared with controls. At the genus level, AE infection led to a rapid depletion of Ligilactobacillus and Lactobacillus between 3 and 6 months, while Akkermansia abundance significantly increased. Histopathological examination of intestinal tissue further demonstrated severe mucosal damage, including villous atrophy, reduced crypt depth, a pronounced decrease in Paneth cell density (P < 0.01), and reduced goblet cell counts (P < 0.05), collectively indicating compromised intestinal barrier integrity.

Conclusion

AE infection induces progressive gut microbiota dysbiosis and compromises intestinal barrier integrity. The specific microbial shifts, particularly the depletion of Ligilactobacillus and enrichment of Akkermansia, represent promising diagnostic biomarkers and potential targets for probiotic supplementation or microbial modulation. To further clarify their roles, future research should incorporate multi-omics strategies, including metagenomics and metabolomics, within larger cohorts to better characterize microbiota-host metabolic interactions and to validate stage-specific microbial biomarkers in AE.