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Fig. 11 Pharmacologic inhibition of neutrophil elastase in ATP7B-KO mice increases liver N2-neutrophil polarization and aggravates liver pathology. (A) Flow cytometric analysis of N1 (CD11b+Ly6G+NOS2+) and N2 (CD11b+Ly6G+CD206+) neutrophil population in total CD11b+Ly6G+ cells derived from the livers of wild-type and ATP7B-KO mice treated with/without GW311616A. (B) Flow cytometric quantification of CD11b+Ly6G+ neutrophils from wild-type and ATP7B-KO mice livers treated with/without GW311616A. (C) Flow cytometric quantification of liver N1 and N2 neutrophils from wild-type and ATP7B-KO mice treated with/without GW311616A. (B and C) n = 6 mice/group, unpaired 2-tailed t test. ∗P < .05, ∗∗P < .01, and ∗∗∗P < .001. Serum activities of (D) ALT, (E) AST, (F) HDL-C, and (G) TChol in wild-type and ATP7B-KO mice treated with/without GW311616A. n = 6 mice/group. ∗∗P < .01, ∗∗∗P < .001. (H) Liver body ratio in wild-type and ATP7B-KO mice treated with/without GW311616A. n = 6 mice/group. ∗∗∗P < .001. (I) Liver Cu content in wild-type and ATP7B-KO mice treated with/without GW311616A. n = 4 mice/group. ∗∗∗P < .001. (J) Representative H&E images in liver sections from wild-type and ATP7B-KO mice treated with/without GW311616A. Scale bar: 50 μm. WT, wild-type.