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. 2023 Oct 3;13:186. doi: 10.1186/s13578-023-01109-0

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — DCA administration enhances Th17 immune response and exacerbates TNBS-induced colitis. a Animal treatment procedure (n = 7 per group). b Representative HE staining and c histological score of colon sections from ND, DCA, ND + TNBS and DCA + TNBS treated mice (n = 4–6). Scale bar, 100 µm (×200) and 50 µm (×400). d The percentage of IL-17-producing cells from mesenteric lymph nodes of ND, DCA, ND + TNBS and DCA + TNBS treated mice. e RORγt (green) and DAPI (blue) immunofluorescence analysis of colon sections from ND, DCA, ND + TNBS and DCA + TNBS treated mice (Scale bar, 50 µm). ***p < 0.001; ****p < 0.0001 compared to the normal diet control mice. ^##p < 0.01 compared to the DCA + TNBS treated mice. One-way ANOVA with Newman-Keuls multiple comparisons test (c) was used. Data are expressed as mean ± SEM from at least three independent experiments or representative data (b, d, e)