摘要：

To The Editors, We thank Sitkin et al. for their interest on our study and their valuable comments.1 The authors speculated that the microbiota changes observed in our study by the addition of butyrate to conventional therapy in patients with IBD could be explained by the activation of epithelial peroxisome proliferator-activated receptor-gamma (PPAR-gamma) signaling, the generation of Treg cells in the colonic lamina propria, the restore of Thl7/Treg balance by inhibiting histone deacetylase, and the enhancement of epithelial barrier function and intestinal homeostasis through hypoxia-inducible factor stabilization. Thus, recovering the anaerobic microbial pool and restoring gut eubiosis can contribute to the improvement of inflammation.

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