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. 2018 Apr 11;9:1393. doi: 10.1038/s41467-018-03764-1

Fig. 1.

Fig. 1

Mice with genetic Ccr2 deficiency are protected from PNAC. a Peripheral serum aspartate-aminotransferase (AST), alanine-aminotransferase (ALT), and total bile acid concentrations in completely unmanipulated mice (chow), DSS-pretreated mice without any further manipulation, (DSS/chow) wild-type (WT) DSS-pretreated mice infused with PN (DSS/PN), PN infused wild-type mice without DSS pretreatment (PN only), and Ccr2−/− DSS-pretreated mice infused with PN (Ccr2−/− DSS/PN). b Liver mRNA from the same groups of mice as in a of genes encoding BSEP (Abcb11), MRP2 (Abcc2), and FXR (Nr1h4) and c liver mRNA from DSS/PN WT and Ccr2−/− mice of genes encoding CD11b (Itgam), Ly6C, CCR2, and F4/80 (Emr1). d Representative liver immunohistochemistry for F4/80 from chow, DSS/chow, and DSS/PN mice (black arrows point to F4/80+ cells). *p < 0.05 vs. all other groups by one-way ANOVA and Tukey's correction (a and c). *p < 0.05 vs. chow, PN only, Ccr2−/− DSS/PN; #p < 0.05 vs. chow by one-way ANOVA and Tukey's correction (b). Data are depicted from individual mice for serum analysis and means from PCR triplicates from individual mice for gene expression data±SEM