Figure 4.

L. intestinalis‐associated RA reduced C/EBPA‐driven SAA production in RAR‐α‐mediated manner. A) Quantification of RA was performed in the feces of acute DSS‐treated mice with PBS or L. intestinalis (L. int) gavage (n = 5). B–F), The pathology of acute colitis and related gene expressions were evaluated between DSS‐treated mice with vehicle (Veh) or RA gavage, by disease activity index (B), colon length (C), pathological scores (D), colonic expression of Saa1, Saa2, and Cebpa (E), and frequencies of Th17 cells (F) (n = 5). G) 2 groups were fed with AIN‐93G as a control diet (Ctrl). Three groups were fed with a vitamin A‐deficient diet (VAL). Pretreatment with gavage of PBS, L. int, or L. int+RA was started on the 7th day before DSS treatment and until the end of the experiment. All mice received a 6‐day 3% DSS treatment. H,I) The pathology of acute colitis was evaluated among Ctrl or VAL‐fed mice with respective gavage, by disease activity index (H) and colon length (I) (n = 5). J–L), The pathology of acute colitis and related gene expressions were evaluated between DSS‐treated mice with vehicle RA or RA+AGN193109 (AGN) administration, by disease activity index (J), colon length (K), and Cebpa expression (L) (n = 5). M) In HT29 cells treated by siRARA, the effect of RA on the expression of C/EBPA was analyzed. Error bars indicate mean ± SEM. ns, no significance; ^* p < 0.05; ^** p < 0.01; ^*** p < 0.001; ^**** p < 0.0001. p values were based on Student's t‐test and one‐way ANOVA with post‐hoc test.