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. 2021 Jul 22;11:15007. doi: 10.1038/s41598-021-94572-z

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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 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/.

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C. butyricum upregulated IL-17A in the cLP to increase IgA production under CDI. (A) Experimental design of fidaxomicin and CBM 588 administration with/without anti-IL-17A antibody in 9- to 10-week-old ICR Swiss mice. (B) Assessment of C. difficile in feces at day 8 and 10. 1: combination (CBM 588 + fidaxomicin) group (Combination), 2: combination group + anti-IL-17A antibody. The testing detectable level is above 2.0 (log amount) per gram of feces, data shown as mean ± SD (n = 5–10 per group). (C) Tumor necrosis factor-α (TNF-α) and (D) Immunoglobrin A (IgA) protein concentrations in mice colon tissue detected at day 8. All values are mean ± SD (n = 5–10).