We read with interest the article by Li et al.1 The authors demonstrated that intraportal transplantation of human bone marrow mesenchymal stem cells (hBMSCs) in pigs with fulminant hepatic failure (D-galactosamine model), significantly improved their long-term survival (87%) compared to both peripheral vein transplantation and sham groups (0%). One of the most interesting findings is that 30% of the recipient liver was repopulated by transplanted hBMSC-derived hepatocytes in surviving animals 2 to 10 weeks post-transplantation. We also learn from this study that hBMSC-derived hepatocytes were well differentiated and expressed hepatocyte-specific markers for albumin, CK8, G6PD, and HNF-1α. In addition, high levels of human-derived albumin were identified in the pig sera; 2.02 ± 0.35 g/L and 3.92 ± 0.5 g/L at week 2 and week 10, respectively. We wonder, and as reported by others, that mature hepatocyte should also express human leukocyte antigen-1 triggering host immune response leading to xenograft rejection.2-4 Do the authors have experimental data to show that hBMSC-derived hepatocytes did not trigger an immune response in these animals?
The authors mention that both treated and control groups did not receive any medications or infusions. Usually, in fulminant hepatic failure patients, complications like hypoglycemia, dyselectrolytemia, and renal dysfunction are very common. Data on blood glucose, serum sodium, and renal function would be of interest in all 3 groups to understand the severity of liver failure, particularly if we are contemplating translation of this work to humans.