The Effects of Sishen Wan on T Cell Responses in Mice Models of Ulcerative Colitis Induced by Dextran Sodium Sulfate.

Evid Based Complement Alternat Med

Liuzhou Key Laboratory for Infectious Disease Immunology Research, Guangxi Health Commission Key Laboratory for Clinical Biotechnology, Liuzhou People's Hospital Affiliated to Guangxi Medical University, Liuzhou 545006, China.

Published: December 2021

Currently, it is unclear whether Sishen Wan (SSW) could modulate the balance of Th1 cells, Th17 cells, and Tregs and we evaluated the effects of SSW on T cell responses in mice models of ulcerative colitis (UC). The mice models of acute UC (4% dextran sodium sulfate (DSS), 8 days) and chronic UC (3% DSS, 16 days) with SSW were assayed. Colon tissues were collected for immunohistochemical analysis, enzyme linked immunosorbent assay (ELISA), and flow cytometry (FCM). The expressions of cytokines associated with Tregs, transcription factors of Th17 cells, the frequencies of Th1 cells, Th17 cells, and Tregs, and the functional plasticity of Th17 cells were detected. The frequency of IFN- T cells was not changed significantly with SSW treatment in acute DSS. In chronic models, the frequency of IFN- T cells was downregulated with SSW. Meanwhile, the levels of RORt and the frequency of IL-17A Th17 cells showed no significant differences after SSW treatment. Despite no significant effect on the transdifferentiation of Th17 cells in chronic UC models, SSW transdifferentiated Th17 cells into IL-10 Th17 cells and downregulated IFN- Th17 cells/IL-10 Th17 cells in acute DSS. Moreover, there were no significant changes of cytokines secreted by Tregs in acute DSS after SSW treatment, but SSW facilitated the expressions of IL-10 and IL-35, as well as development of IL-10 Tregs in chronic DSS. SSW showed depressive effects on the immunoreaction of Th17 cells and might promote the conversion of Th17 cells into IL-10 Th17 cells in acute UC, while it inhibited the excessive reaction of Th1 cells, facilitated the development of Tregs, and enhanced the anti-inflammatory effects in chronic UC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8702314PMC
http://dx.doi.org/10.1155/2021/9957709DOI Listing

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