Pretreatment with bacterial components promotes DSS-injured colonic epithelial repair through the activation of STAT-3.

Bacterial protection and epithelial repair are important against inflammatory bowel disease (IBD). The present study was designed to examine the effects of different bacterial components on the repair of normal and dextran sodium sulfate (DSS)‑treated colonic epithelial cells and the corresponding mechanisms. Human colonic epithelial cells (HT‑29) were pretreated with various doses of LPS or CpG‑dsDNA for 24 h and then treated with or without DSS for another 24 h. The epithelial repair was assessed by video analyses following mechanical injury. The epithelial expression of cluster of differentiation (CD)40 was assayed using flow cytometeric analysis. The production of interleukin (IL)‑6 and tumor necrosis factor (TNF) in the cell culture medium were measured using ELISA. The expression of p38 mitogen‑activated protein kinase (MAPK) and signal transducer and activator of transcription (STAT)‑3 were examined using western blot analysis and reverse transcription‑quantitative polymerase chain reaction analysis. MAPK and STAT‑3 inhibitors were also administrated to observe signaling‑mediated repair. The results showed that pretreatment with lipopolysaccharide (LPS) or CpG‑dsDNA promoted epithelial repair of the DSS‑treated cells. The promoting effects were associated with the downregulation of CD40 molecules, inhibition of the p38 MAPK/TNFα pathway and activation of the STAT3/IL‑6 pathway. The STAT3 inhibitor abrogated the protective effects of LPS and CpG‑dsDNA on wound repair. These results demonstrated that LPS and CpG‑dsDNA induced preadaptation to DSS injury. This preadaptation was accompanied by the activation of STAT‑3. Thus, bacterial components may be used as a strategy for the therapeutic prevention of IBD.