Published online Aug 14, 2023. doi: 10.3748/wjg.v29.i30.4657
Peer-review started: May 22, 2023
First decision: June 20, 2023
Revised: July 3, 2023
Accepted: July 11, 2023
Article in press: July 11, 2023
Published online: August 14, 2023
Processing time: 79 Days and 23.3 Hours
It is well known that microbiota dysbiosis contributes to the occurrence of inflammatory bowel disease (IBD). Fecal microbiota transplantation (FMT) has shown promising therapeutic effects on both clinical and basic studies of ulcerative colitis (UC). Substantial evidence supports a negative pro-inflammatory role of Toll-like receptor 4 (TLR4) signaling pathway in IBD. However, it remains unknown whether this modulation is also involved in the treatment of FMT on UC.
FMT treats other diseases by regulating the TLR4 signaling pathway. Previous studies have shown that the expression of TLR4 is higher in the intestinal mucosa of patients with effective FMT and lower in patients with poor FMT. We speculate that the TLR4 signaling pathway may be involved in the therapeutic mechanism of FMT on IBD.
To clarify the necessity of TLR4 signaling pathway in FMT on regulating gut microbiota in dextran sodium sulphate (DSS)-induced colitis.
Experimental colitis was constructed in wild-type (WT) and TLR4-knockout (KO) mice and fecal microbiota was transplanted by gavage. Colon inflammation severity in mouse model was measured by disease activity index (DAI) score and hematoxylin and eosin (H&E) staining. Gut microbiota alteration was analyzed through 16S ribosomal RNA sequencing. The difference of gene expression in mouse colon was obtained by transcriptome sequencing of colon tissue.
In KO mice treated with FMT or water, these two groups displayed indistinguishable body weight loss, colon length, DAI score, and histology score, which showed that FMT could hardly alter the disease progress in KO mice. Next, compared with WT mice, the scores of DAI and colon histology clearly decreased in the KO-DSS group. KO mice experienced enhanced resistibility to DSS-induced colitis. There was a significant difference in the microbiota structure between KO and WT mice. Akkermansia was the dominant genus in healthy KO mice. But unexpectedly, after treatment with FMT, the relative abundance of Akkermansia decreased, while the level of Lactobacillus in the intestine of mice was maintained. The ineffectiveness in KO mice after FMT was related to the decrease of Akkermansia. GO enrichment analysis showed that DEGs between each group were mainly involved in cytoplasmic translation and cellular response to DNA damage stimulus. Finally, we listed the top nine genes related to Akkermansia.
FMT may ameliorate DSS-induced colitis by regulating the TLR4 signaling pathway.
This study provides new insights into the underlying mechanisms of FMT as a treatment for UC, which greatly helps to optimize FMT treatment in the future.