FIGURE 10.

Schematic representation of microbial metabolite butyrate-induced intestinal adaptation via the immune response to weaning stress. (A) Weaning stress-induced intestinal dysfunction: at the first week post-weaning (transition from lactation to weaning), weaning stress induces significant alterations of core OTUs and alpha diversity, especially increases in two dominant taxonomic groups (i.e., Erysipelotrichaceae and Lachnospiraceae). These changes result in decreased butyrate production and decreased expression of its receptor (GPR-43), which contributes to the onset of apoptosis and the inhibition of proliferation along the crypt-villus axis via inducing increased pro-inflammatory cytokines. As a result, pronounced shifts of the intestinal structure and function toward post-weaning intestinal dysfunction (increased crypt-depth) occur, which significantly decrease digestive-enzyme activities (i.e., CK and LDH) and growth check (i.e., low feed intake and body weight). (B) Self-repairing mechanism-induced jejunal adaptation toward health status: at the second week post-weaning (transition from weaning to post-weaning), increasing the relative abundances of Lactobacillaceae and Ruminococcaceae are accompanied by decreased in core OTUs and the alpha diversity of bacteria community. These changes stimulate butyrate production and expression of its receptor, which lead to the inhibition of apoptosis and the stimulation of proliferation via decreased pro-inflammatory cytokines, thereby promoting the development of post-weaning intestinal environment toward health status. OTUs, operational taxonomic units; CK, creatine kinase; LDH, lactate dehydrogenase.