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. 2021 Sep 30;13:31. doi: 10.1038/s41368-021-00136-2

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© The Author(s) 2021

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — P. gingivalis- and comΔppad-exacerbated UC is associated with an imbalance in Th17/Tregs. a, b Flow cytometric analysis and bar chart showing that compared with Δppad, P. gingivalis and comΔppad induced the transformation of CD4⁺ T cells into proinflammatory Th17 cells and simultaneously inhibited the generation of Tregs (P < 0.05), but no difference was observed between mice administered Δppad and DSS and mice with colitis administered physiological saline (P > 0.05). c ELISA showing that compared with Δppad, P. gingivalis and comΔppad administration caused the increased expression of IL-17 and decreased expression of IL-10 in serum (P < 0.05). The expression levels of the two cytokines were similar in the mice administered Δppad and DSS mice and the mice with colitis (P > 0.05). All indicators were measured with six replicates. The data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.000 1 by independent 2-tailed Student’s t test and one-way ANOVA combined with Mann-Whitney U test