Escherichiacoli promotes DSS‑induced murine colitis recovery through activation of the TLR4/NF‑κB signaling pathway.

Abstract

Increasing evidence suggests that intestinal microbiota have critical function in the pathogenesis of inflammatory bowel disease. This present study investigated the effects of Escherichia coli (E. coli) in mice with dextran sulfate sodium (DSS)-induced colitis. Furthermore, Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) gene expression was measured by reverse transcription-quantitative polymerase chain reaction. In total, two experiments were performed. In the first experiment, four groups were established in BALB/c mice: i) Group A, control (no treatments); ii) group B, DSS-induced colitis; iii) group C, DSS-induced colitis bacteria depleted (BD) mice; and iv) group D, E. coli-treated DSS-induced colitis BD mice. In the second experiment, there were three groups: i) Group A1, control C57BL/6 mice; ii) group B1, E. coli-treated DSS-induced colitis BD C57BL/6 mice; and iii) E. coli-treated DSS-induced colitis BD TLR4−/− mice. Clinical outcomes, colon and immune histopathology and tissue myeloperoxidase activity were assessed. Mice with DSS-induced colitis that were treated with E. coli exhibited enhanced recovery, with significantly improved clinical and histological scores compared with the DSS only group. The mRNA expression of TLR4 and NF-κB in the E. coli-treated group was also significantly higher. These effects were abolished in TLR4−/− mice, suggesting that E. coli may have promoted recovery through the TLR4 pathway. The present study indicated that E. coli promoted recovery from DSS-induced colitis in mice, potentially through activation of the TLR4/NF-κB signaling pathway.