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. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: Hepatology. 2018 Mar 25;67(5):1903–1919. doi: 10.1002/hep.29652

Figure 8. Inflammasome activation is increased in FPC-defective cholangiocytes and is responsible for IL-1β secretion.

Figure 8

A) Western blot analysis for phosphorylated p65 fraction of NF-kB (Ser276 and Ser536) in nuclear cell extracts showed increased phosphorylated p65 in FPC-defective (FPC−) as compared to WT cholangiocytes (n=5). B) Similarly, cleaved caspase-1 (p10) was increased in FPC-defective cholangiocytes as compared to WT (n=6). C) Nlrp3 gene expression was increased in FPC-defective cholangiocytes compared to WT (n=8). D) Treatment with an inhibitor of NLRP3 canonical and non-canonical activation (MCC950) decreased IL-1β protein levels in FPC-defective cholangiocytes compared to WT (n=6). (*p<0.05, Students Ttest or ANOVA with post hoc corrections). NLRP3: Nod-like receptors, pyrin domain containing 3. FPC−: Fibrocystin-defective cholangiocytes.