Background: Emerging evidence has demonstrated that fecal microbiota transplantation (FMT) has a promising therapeutic effect on mice with experimental colitis and patients with ulcerative colitis (UC), although the mechanism of FMT is unclear.
Aim: To evaluate the protective effect of FMT on UC and clarify its potential dependence on the gut microbiota, through association analysis of gut microbiota with colon transcriptome in mice.
Methods: Dextran sodium sulfate (DSS)-induced experimental colitis was established and fecal microbiota was transplanted by gavage. Severity of colon inflammation was measured by body weight, disease activity index, colon length and histological score. Gut microbiota alteration was analyzed through 16S ribosomal ribonucleic acid sequencing. The differentially expressed genes (DEGs) in the colon were obtained by transcriptome sequencing. The activation status of colonic T lymphocytes in the lamina propria was evaluated by flow cytometry.
Results: Compared with the DSS group, the weight loss, colon length shortening and inflammation were significantly alleviated in the FMT group. The scores of disease activity index and colon histology decreased obviously after FMT. FMT restored the balance of gut microbiota, especially by upregulating the relative abundance of and downregulating the relative abundance of and . In the transcriptomic analysis, 128 DEGs intersected after DSS treatment and FMT. Functional annotation analysis suggested that these DEGs were mainly involved in T-lymphocyte activation. In the DSS group, there was an increase in colonic T helper CD4 and T cytotoxic CD8 cells by flow cytometry. FMT selectively downregulated the ratio of colonic CD4 and CD8 T cells to maintain intestinal homeostasis. Furthermore, was significantly related to inflammation-related genes including , and .
Conclusion: FMT ameliorated DSS-induced colitis in mice regulating the gut microbiota and T-cell modulation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8173381 | PMC |
| http://dx.doi.org/10.3748/wjg.v27.i21.2834 | DOI Listing |
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