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. 2022 Nov 3;13:6615. doi: 10.1038/s41467-022-34260-2

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© The Author(s) 2022

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. 2 — Panel A displays genes encoding for antibiotic resistance. Panel B displays genes encoding for bacteriocins. Panel C displays genes encoding for toxins/hemolysins/cytolysins. Panel D displays the genes responsible for bile acid conversion, as well as butyrate-related enzymes and desaminotyrosine. Genes in Panels A, B, D were quantified using RPKM values (shades of pink) while toxin genes in Panel C were determined as presence/absence (blue/white). Gray boxes show missing data. P-values and adjusted p-values (via Benjamini-Hochberg method) were obtained from Wilcoxon rank-sum, two-tailed tests (A, B, D) and a two-tailed, chi-squared test (C) and are shown as shading from non-significant (gray) to statistically significant (green). n = 71 independent samples from patients.