Effect of Clostridium butyricum and its components in different concentrations on epithelial-mesenchymal transition of ulcerative colitis

Objective: To investigate the effect and potential mechanism of Clostridium butyricum (CB) in different concentrations on epithelial-mesenchymal transition (EMT) of ulcerative colitis. Methods: Fifty C57BL/6 mice were randomly divided as a control group, a DSS group, a low-dose, a middle-dose and a high-dose CB treated group. DAI, colon length, and tissue damage for each group was assessed. Expression of E-cadherin and Vimentin in the colon was detected by real-time qPCR and IHC. In vitro, the control, TGF-beta 1, low-dose, high-dose supernatant and dead CB groups were monitored for loss of cell polarity and expression of phenotype by real time qPCR and Western blotting. Results: Compared to the control group, DAI and colon length in the DSS group was significantly deteriorated (P<0.05) with most crypt loss and infiltrating inflammatory cells as significantly down-regulation of E-cadherin and up-regulation of Vimentin by IHC staining (P<0.05). Not like the high-dose CB group, DAI, colon length and tissue damage in the low-dose and middle-dose CB group was critically ameliorated on the final experimental day (P<0.05) with up-regulation E-cadherin and down-regulation vimentin. In vitro, supernatant and the dead CB group, especial the high-dose dead CB, could prevent loss of cell polarity. Dead and high-dose supernatant of CB could significantly down-regulate vimentin mRNA (P<0.05), when supernatant of both CB groups could up-regulate expression of E-cadherin mRNA by regulating TGF-beta 1 mRNA. At the protein level, high-dose supernatant of CB could increase expression of E-cadherin and decrease that of vimentin. Conclusion: Clostridium butyricum could dose-dependently suppress experimental colitis because of its components inhibiting EMT undergoing down-regulation TGF-beta 1.