Clostridium butyricum protects the ileal barrier in mice by regulating the farnesoid X receptor signaling pathway

Abstract

Background

The intestinal barrier has an important role in maintaining homeostasis. The aim of this study was to determine the protective effect of Clostridium butyricum (CBM) on small intestinal barrier damage in mice and the role of farnesoid X receptor (FXR) in regulating the intestinal barrier by C. butyricum.

Methods and results

A model of small intestinal injury induced by dextran sulfate sodium (DSS) was constructed to detect repair of intestinal barrier damage after feeding with C. butyricum. In the DSS model group, expression of the tight junction protein (TJP) was significantly decreased and expression of inflammatory factors was significantly increased. TJP expression was significantly increased and inflammatory factor expression was significantly decreased after C. butyricum feeding, which indicated that intestinal barrier function was repaired. In addition, inhibition of FXR expression as well as the downstream signaling pathways were demonstrated in the DSS model group. FXR and its downstream signaling pathways were significantly upregulated after feeding with C. butyricum. Then, intestinal barrier function was evaluated by constructing an intestinal-specific FXR knockout (KO) DSS model in mice. Suppression of TJP and upregulated expression of inflammatory factors were detected in the KO DSS group but there was no significant difference in the expression of TJP and inflammatory factors after C. butyricum feeding. Furthermore, there was no significant difference in FXR downstream signaling pathway expression after C. butyricum feeding compared to the KO DSS group. C. butyricum supernatants (CSs) upregulated the FXR signaling pathways in vitro. CSs did not activate the FXR signaling pathway when FXR was suppressed.

Conclusions

C. butyricum supplementation effectively ameliorated DSS-induced intestinal barrier disruption. C. butyricum may have a protective effect on the small intestine through the FXR signaling pathway.