<i>Clostridium Butyricum</i> ZJU-F1 Benefits the Intestinal Barrier Function and Immune Response Associated with Its Modulation of Gut Microbiota in Weaned Piglets

• Main Authors: Jie Fu, Tenghao Wang, Xiao Xiao, Yuanzhi Cheng, Fengqin Wang, Mingliang Jin, Yizhen Wang, Xin Zong
• Format: Article
• Language: English
• Published: MDPI AG 2021-03-01
• Series: Cells
• Subjects: <i>C. butyricum</i> ZJU-F1; microbiota; weaning piglets; intestinal barrier; TLR2
• Online Access: https://www.mdpi.com/2073-4409/10/3/527

This study investigated the effects of dietary <i>C. butyricum</i> ZJU-F1 on the apparent digestibility of nutrients, intestinal barrier function, immune response, and microflora of weaned piglets, with the aim of providing a theoretical basis for the application of <i>Clostridium butyricum</i> as an alternative to antibiotics in weaned piglets. A total of 120 weanling piglets were randomly divided into four treatment groups, in which piglets were fed a basal diet supplemented with antibiotics (CON), <i>Bacillus licheniformis</i> (BL), <i>Clostridium butyricum </i>ZJU-F1 (CB), or <i>Clostridium butyricum</i> and <i>Bacillus licheniformis</i> (CB-BL), respectively. The results showed that CB and CB-BL treatment increased the intestinal digestibility of nutrients, decreased intestinal permeability, and increased intestinal tight junction protein and mucin expression, thus maintaining the integrity of the intestinal epithelial barrier. CB and CB-BL, as exogenous probiotics, were also found to stimulate the immune response of weaned piglets and improve the expression of antimicrobial peptides in the ileum. In addition, dietary CB and CB-BL increased the proportion of <i>Lactobacillus.</i> The levels of butyric acid, propionic acid, acetic acid, and total acid were significantly increased in the ceca of piglets fed CB and CB-BL. Furthermore, we validated the effects of <i>C. butyricum </i>ZJU-F1 on the intestinal barrier function and immune response in vitro and found <i>C. butyricum</i> ZJU-F1 improved intestinal function and enhanced the TLR-2-MyD88-NF-κB signaling.