WZ1 Inhibits the Inflammatory Injury of Mouse Jejunum Caused by Enterotoxigenic K88 by Regulating the TLR4/NF-κB/MyD88 Inflammatory Pathway and Gut Microbiota.

Replacing antibiotics with probiotics has become an important way to safely and effectively prevent and treat some gastrointestinal diseases. This study was conducted to investigate whether WZ1 (L.S) could reduce the inflammatory injury to the mouse jejunum induced by (ETEC) K88. Forty Kunming mice were randomly divided into four groups with 10 mice in each group. From day 1 to day 14, the control group and the group were administered with normal saline each day, while the L.S group and the L.S + group were gavaged with WZ1 1 × 10 CFU/mL each day. On the 15th day, the group and the L.S + group were intragastrically administered ETEC K88 1 × 10 CFU/mL and sacrificed 24 h later. Our results show that pretreatment with WZ1 can dramatically protect the jejunum morphological structure from the changes caused by ETEC K88 and relieve the morphological lesions of the jejunum, inhibiting changes in the mRNA expressions of , and and the protein expressions of TLR4, NF-κB and MyD88 in the intestinal tissue of mice caused by ETEC K88. Moreover, pretreatment with WZ1 also increased the relative abundance of beneficial genera such as and and decreased the abundance of harmful genera such as and in the gut. These results demonstrate that WZ1 can inhibit the inflammatory damage caused by ETEC K88 in mouse jejunum by regulating the TLR4/NF-κB/MyD88 inflammatory pathway and gut microbiota.