Fig. 2.

Injection of AAMs reduces several serum proinflammatory cytokines following APAP-ALI.

(A) Serum concentrations of proinflammatory cytokines measured in APAP-ALI mice receiving indicated treatments (n = 10–12 per group; some sera had undetectable IL-12p70). (B) IL-6 levels in liver homogenates from APAP-ALI mice receiving indicated treatments (n = 5–11 per group) (C) Relative expression of indicated genes (using 2^−ΔΔCT method; standardised to PBS-treated controls, after GAPDH normalisation) in liver tissue of APAP-ALI mice receiving indicated treatments (n = 6–10 per group). In A–C, white circles — individual vehicle controls; grey circles — cell-transfer reference group; blue circles — AAM-treated mice. (D) Study design: Plasma biomarkers were measured daily in APAP-ALI mice following PBS/AAM-treatment. (E/F/G) Plasma biomarkers (left panels) and change in plasma biomarkers from point-of-treatment (right panels) for plasma ALT activity (E), AST activity (F), and miR-122 levels (G). Shaded area represents treatment phase. Grouped values represents mean ± SD for AAM-treatment (blue) and PBS-treatment (white). Plasma miR-122 levels are presented as relative quantitation (using 2^-ΔΔCT method; standardised to pre-APAP-ALI levels (−96 h), after let-7d normalisation). p values provided in panels; n.s., not significant, ∗p <0.05, ∗∗p <0.01. Kruskal-Wallis tests for A/B/C (Csf1/Ccl5), one-way ANOVA for C (Tgfb, Il6, Cxcl1), mixed-effects model for (E/F/G). AAMs, alternatively activated macrophages; ALI, acute liver injury; ALT, alanine aminotransferase; APAP, acetaminophen; APAP-ALI, APAP-induced ALI.