Figure 8

Proposed mechanisms to show colonization resistance induced by Clostridium butyricum MIYAIRI 588 strain (CBM 588) against Clostridioides difficile infection. Not only CBM 588 modulated gut microbiome, CBM 588 negatively modulated gut succinate levels to prevent C. difficile proliferation and downregulate tumor necrosis factor-α (TNF-α) producing macrophages in the colon lumina propria (cLP), resulting in a significant decrease in colon epithelial damage. Additionally, CBM 588 upregulated T cell-dependent pathogen specific immunoglobulin A (IgA) via interleukin (IL)-17A producing CD4+ cells and plasma B cells in the cLP, and Th17 cells in the cLP enhanced the gut epithelial barrier function (as shown to the right). SUCNR1: succinate receptor 1.