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. 2022 Dec 15;191(2):321–331. doi: 10.1093/toxsci/kfac132

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© The Author(s) 2022. Published by Oxford University Press on behalf of the Society of Toxicology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — Increased expression of proinflammatory genes in DSS-exposed Ahr^dbd/dbd compared with wild-type mice. Intestinal mRNA expression levels of (A) Cyp1a1, (B) Il-1b, (C) Il-6, (D) Il-17, (E) Ptgs2, (F) Lcn2 (G) Cxcl1, (H) Cxcl2, (I) Cxcl5, (J) Il-21, (K) Il-10, and (L) Il-22 in colon tissue isolated from Ahr^+/+ and Ahr^dbd/dbd mice that were not exposed to DSS (No DSS) or exposed to 2% DSS in their drinking water. The relative mRNA levels of the indicated genes were determined with RT-qPCR. **p < .05 Student’s t-test compared with genotype and treatment-matched Ahr^+/+ mice. *p < .05 2-way ANOVA compared with genotype-matched and DSS-treated animals. ^#p < .05 2-way ANOVA compared with treatment-matched Ahr^+/+ mice. Abbreviation: DSS, dextran sulfate sodium.