| First Author | Lu J | Year | 2019 |
| Journal | Mol Med Rep | Volume | 19 |
| Issue | 3 | Pages | 2021-2028 |
| PubMed ID | 30664156 | Mgi Jnum | J:295626 |
| Mgi Id | MGI:6454137 | Doi | 10.3892/mmr.2019.9848 |
| Citation | Lu J, et al. (2019) Escherichia coli promotes DSSinduced murine colitis recovery through activation of the TLR4/NFkappaB signaling pathway. Mol Med Rep 19(3):2021-2028 |
| abstractText | 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, Tolllike receptor 4 (TLR4) and nuclear factorkappaB (NFkappaB) gene expression was measured by reverse transcriptionquantitative 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, DSSinduced colitis; iii) group C, DSSinduced colitis bacteria depleted (BD) mice; and iv) group D, E. colitreated DSSinduced colitis BD mice. In the second experiment, there were three groups: i) Group A1, control C57BL/6 mice; ii) group B1, E. colitreated DSSinduced colitis BD C57BL/6 mice; and iii) E. colitreated DSSinduced colitis BD TLR4/ mice. Clinical outcomes, colon and immune histopathology and tissue myeloperoxidase activity were assessed. Mice with DSSinduced 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 NFkappaB in the E. colitreated 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 DSSinduced colitis in mice, potentially through activation of the TLR4/NFkappaB signaling pathway. |
