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. Author manuscript; available in PMC: 2018 Aug 21.
Published in final edited form as: Pediatr Res. 2018 Feb 21;83(5):1031–1040. doi: 10.1038/pr.2018.14

Figure 5.

Figure 5

The ability of LCA to diminish LPS-induced production of IL-6 in intestinal tissues is PXR-dependent. (A) Expression levels of LPS-induced transcripts for IL-6 (i) and TNFα (ii) in IEC-6 enterocytes pretreated or not with 100 µM of LCA (24 hrs) in the absence or presence of PXR siRNA or scrambled siRNA (200 µM). (B) Expression levels of LPS-induced transcripts for IL-6 (i and ii) and TNF-α (iii) in intestinal organoids obtained from WT or PXR−/− mice that were pretreated or not with 100 µM of LCA (16 hrs). Exposures to LPS were for 2 hr at 1µg/ml (A) or 4hr at 10 µg/ml (B). Results shown are for experiments performed in triplicate. Fold changes were calculated by comparing to untreated cells or organoids and normalized to β-actin. * P ≤ 0.05, **P ≤ 0.01, by ANOVA with Tukey’s multiple comparison test (A), or unpaired t test (B); n.s., not significant.