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<p><i>Clostridium perfringens</i> type C (<i>Cp</i>C)-induced piglet diarrhea is a major challenge in the swine industry. This study aimed to investigate the protective effects of fecal microbiota transplantation (FMT) from Hezuo pigs against intestinal injury in Duroc×Landrace×Yorkshire (DLY) suckling piglets infected with <i>Cp</i>C. Piglets were divided into two groups, including <i>Cp</i>C-challenged control group and FMT-treatment group, which received fecal suspension from Hezuo pigs prior to infection. Morphological, immunological, microbiomic, and metabolomic analyses were conducted after post-infection. The results demonstrated that FMT significantly alleviated jejunal damage, leading to a significant increase in jejunal villus height and a significant decrease in crypt depth (<i>P</i> &lt; 0.01). The intervention elevated the number of goblet cells (<i>P</i> &lt; 0.05) and upregulated the expression of tight junction protein genes <i>Occludin</i>, <i>ZO-1</i>, <i>Claudin-1</i> and the anti-inflammatory cytokine IL-10, while significantly reducing the levels of pro-inflammatory cytokines TNF-α and IL-6 (<i>P</i> &lt; 0.05). FMT enriched beneficial genera such as <i>Akkermansia</i>, <i>Rothia</i>, <i>Peptococcus</i>, and <i>Proteocatella</i>, and increased the levels of the sphingolipid metabolite ceramide (d18:1/18:0). Correlation analysis further indicated that these microbiota alterations were positively associated with intestinal barrier repair and anti-inflammatory activity, and were strongly correlated with ceramide (d18:1/18:0) levels. In conclusion, FMT mitigates <i>Cp</i>C-induced intestinal injury by modulating the gut microbiota and metabolome, thereby enhancing intestinal barrier integrity and regulating inflammatory responses. This study provides theoretical support and practical insights for the application of FMT as a promising microbiome-based strategy to control <i>Cp</i>C-associated intestinal diseases in piglets.</p>

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Fecal microbiota transplantation from Hezuo pigs alleviates intestinal inflammatory injury in Clostridium perfringens type C-infected piglets via modulation gut microbiota and intestinal barrier

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月2日

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  • Qiaoli Yang,
  • YuHao Liang,
  • Jing Liu,
  • Rui Jia,
  • Jie Li,
  • ZunQiang Yan

摘要

Clostridium perfringens type C (CpC)-induced piglet diarrhea is a major challenge in the swine industry. This study aimed to investigate the protective effects of fecal microbiota transplantation (FMT) from Hezuo pigs against intestinal injury in Duroc×Landrace×Yorkshire (DLY) suckling piglets infected with CpC. Piglets were divided into two groups, including CpC-challenged control group and FMT-treatment group, which received fecal suspension from Hezuo pigs prior to infection. Morphological, immunological, microbiomic, and metabolomic analyses were conducted after post-infection. The results demonstrated that FMT significantly alleviated jejunal damage, leading to a significant increase in jejunal villus height and a significant decrease in crypt depth (P < 0.01). The intervention elevated the number of goblet cells (P < 0.05) and upregulated the expression of tight junction protein genes Occludin, ZO-1, Claudin-1 and the anti-inflammatory cytokine IL-10, while significantly reducing the levels of pro-inflammatory cytokines TNF-α and IL-6 (P < 0.05). FMT enriched beneficial genera such as Akkermansia, Rothia, Peptococcus, and Proteocatella, and increased the levels of the sphingolipid metabolite ceramide (d18:1/18:0). Correlation analysis further indicated that these microbiota alterations were positively associated with intestinal barrier repair and anti-inflammatory activity, and were strongly correlated with ceramide (d18:1/18:0) levels. In conclusion, FMT mitigates CpC-induced intestinal injury by modulating the gut microbiota and metabolome, thereby enhancing intestinal barrier integrity and regulating inflammatory responses. This study provides theoretical support and practical insights for the application of FMT as a promising microbiome-based strategy to control CpC-associated intestinal diseases in piglets.