Bacillus amyloliquefaciens SC06 Ameliorated Intestinal Mucosal Injury by Regulated Intestinal Stem Cells Proliferation and Differentiation via Activating Wnt/β-Catenin Signal Pathway in Clostridium perfringens-Challenged Mouse

The objective of our study was to verify the intervention effect of <i>Bacillus amyloliquefaciens</i> SC06 on NE by constructing a <i>C. perfringens</i>-induced intestinal damage mouse model. A total of 40 mice were randomly assigned to four treatments: CON (basal diet), CP (basal diet + <i>C. perfringens</i>), SC06 + CP (basal diet + SC06 + <i>C. perfringens</i>) and SC06 (basal diet + SC06). Our findings indicated that SC06 supplementation was effective in maintaining the integrity of the intestinal barrier, enhancing the antioxidant capacity of the intestine, reducing the generation of an inflammatory response, and suppressing enterocyte apoptosis in the presence of <i>C. perfringens</i>. Furthermore, SC06 supplementation enhanced the prefoliation of intestinal stem cells (ISC) and prompted their differentiation into goblet cells and Paneth cells. Moreover, our findings indicate that SC06 promotes the proliferation of <i>C. perfringens</i>-induced jejunum organoids and the expression of genes and proteins associated with ISC differentiation and regeneration. The mechanism by which SC06 modulates ISCs has been validated, and the results align with those obtained in vivo. In conclusion, the findings demonstrated that SC06 stimulates the proliferation and differentiation of ISCs through the activation of the Wnt/β-catenin signaling pathway, thereby accelerating epithelial regeneration and repair.

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Journal
Microorganisms
Published
2025-09-12
DOI
https://doi.org/10.3390/microorganisms13092136
Primary Topic
Cancer Research and Treatments
Type
article
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article

Bacillus amyloliquefaciens SC06 Ameliorated Intestinal Mucosal Injury by Regulated Intestinal Stem Cells Proliferation and Differentiation via Activating Wnt/β-Catenin Signal Pathway in Clostridium perfringens-Challenged Mouse

Haibin Hao, Weiqin Li, Jiemei Fan, Hong-Bin Deng et al.
Microorganisms
Cancer Research and Treatments
article

Bacillus amyloliquefaciens SC06 Ameliorated Intestinal Mucosal Injury by Regulated Intestinal Stem Cells Proliferation and Differentiation via Activating Wnt/β-Catenin Signal Pathway in Clostridium perfringens-Challenged Mouse

Haibin Hao, Weiqin Li, Jiemei Fan, Hong-Bin Deng, Dandong Fang, Si Cheng, Qi Wang
article en

Abstract

The objective of our study was to verify the intervention effect of <i>Bacillus amyloliquefaciens</i> SC06 on NE by constructing a <i>C. perfringens</i>-induced intestinal damage mouse model. A total of 40 mice were randomly assigned to four treatments: CON (basal diet), CP (basal diet + <i>C. perfringens</i>), SC06 + CP (basal diet + SC06 + <i>C. perfringens</i>) and SC06 (basal diet + SC06). Our findings indicated that SC06 supplementation was effective in maintaining the integrity of the intestinal barrier, enhancing the antioxidant capacity of the intestine, reducing the generation of an inflammatory response, and suppressing enterocyte apoptosis in the presence of <i>C. perfringens</i>. Furthermore, SC06 supplementation enhanced the prefoliation of intestinal stem cells (ISC) and prompted their differentiation into goblet cells and Paneth cells. Moreover, our findings indicate that SC06 promotes the proliferation of <i>C. perfringens</i>-induced jejunum organoids and the expression of genes and proteins associated with ISC differentiation and regeneration. The mechanism by which SC06 modulates ISCs has been validated, and the results align with those obtained in vivo. In conclusion, the findings demonstrated that SC06 stimulates the proliferation and differentiation of ISCs through the activation of the Wnt/β-catenin signaling pathway, thereby accelerating epithelial regeneration and repair.

MicroorganismsVol. 13(9)
Nanjing General Hospital of Nanjing Military Command (CN), Institute of Animal Sciences (CN), Zhejiang University (CN), Nanjing University (CN)
Openalex Percentile: Top 72%
Cancer Research and Treatments
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