Skip to main content
. 2017 Jul;153(1):263–276.e8. doi: 10.1053/j.gastro.2017.03.023

Figure 5.

Figure 5

Human and murine sources of soluble sCD80 and sCD86. (A) Hepatocytes were first assessed for apoptosis and necrosis. Apoptotic cells are stained bright green and necrotic bright red. (B) Primary human hepatocytes were tested for their ability to secrete sCD86 hepatocytes after APAP treatment. Supernatants from 24 hours post APAP-treated hepatocytes were assessed by enzyme-linked immunosorbent assays (ELISA) for concentrations of sCD86 (top panel) and for soluble cell death markers (M30 and M65) (bottom panel). (C) Circulating levels of M30 (left panel) and M65 (right panel) in ALF (n = 25), ACLF (n = 20), CLD (n = 15), and sepsis (n = 20) patients determined in sera by ELISA. (D) Representative H&E-stained histology sections of liver tissue from murine model of APAP-induced liver injury highlighting different stages in the evolution and recovery from APAP-induced liver injury. Liver injury initiation (characterized by centrilobular hepatocyte necrosis) (8 hours), peak (24 hours), and resolution (within 5 days). (E) Left: Levels of sCD86 measured in APAP-injury murine sera at 0 hours, 8 hours, 24 hours, 48 hours, and 5 days post APAP-induced liver injury and (right) corresponding alanine aminotransferase (ALT) sera levels (n = 5 per group).