Roseburia intestinalis supernatant ameliorates colitis induced in mice by regulating the immune response

Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD), has a complex etiology that may be associated with dysbiosis of the microbiota. Previously, our study revealed significant loss of Roseburia intestinalis from the gut of untreated patients with CD, and that R. intestinalis exerted anti-inflammatory functions in TNBS-induced colitis; however, the function of R. intestinalis supernatant is unknown. Therefore, LPS-induced macrophages, including RAW264.7 macrophages and bone marrow-derived macrophages were treated with R. intestinalis supernatant. The results indicated that R. intestinalis supernatant suppressed expression of interleukin (IL)-6 and signal transducer and activator of transcription 3 (STAT3) by macrophages. Additionally, these findings were further verified in vivo in DSS- and TNBS-induced mouse models of colitis. It was observed that R. intestinalis supernatant ameliorated IBD colitis by reducing the number of inflammatory macrophages and Th17 cells in the colon, and by downregulating the expression of IL-6 and STAT3. Finally, the non-protein components of R. intestinalis supernatant were examined using gas chromatography-mass spectrometry analysis and identified the presence of short-chain fatty acids. In conclusion, the results of the present study indicated that R. intestinalis supernatant may regulate immune responses and ameliorate colitis.