Fig. 12

Genetic 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 populations in total CD11b+Ly6G+ cells derived from the livers of wild-type and ATP7B-KO mice with/without genetic deletion of neutrophil elastase. (B) Flow cytometric quantification of CD11b+Ly6G+ neutrophils from wild-type and ATP7B-KO mice livers with/without genetic deletion of neutrophil elastase. (C) Flow cytometric quantification of liver N1 and N2 neutrophils from wild-type and ATP7B-KO mice with or without genetic deletion of neutrophil elastase. (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 with/without genetic deletion of neutrophil elastase. n = 6 mice/group. ?P < .05, ??P < .01, and ???P < .001. (H) Liver body ratio in wild-type and ATP7B-KO mice with/without genetic deletion of neutrophil elastase. n = 6 mice/group. ??P < .01, ???P < .001. (I) Liver Cu content in wild-type and ATP7B-KO mice with/without genetic deletion of neutrophil elastase. n = 4 mice/group. ???P < .001. (J) Representative H&E images in liver sections from wild-type and ATP7B-KO mice with/without genetic deletion of neutrophil elastase. Scale bar: 50 ?m. WT, wild-type.