Efficiency of porcine endothelial cell infection with human cytomegalovirus depends on both virus tropism and endothelial cell vascular origin.

Background: Human cytomegalovirus (HCMV) infection or reactivation has been linked to allograft rejection resulting from endothelial injury and immune activation. In pig-to-human xenotransplantation, currently investigated to circumvent the shortage of human organs in transplantation medicine, the porcine endothelium will inevitably be exposed to human pathogens such as HCMV. We investigated the susceptibility of porcine endothelial cells (pEC) to HCMV infection.

Human CMV infection of porcine endothelial cells increases adhesion receptor expression and human leukocyte recruitment.

Background: Potential xenozoonosis is a concern for the clinical application of xenotransplantation. Human cytomegalovirus (HCMV) is one of the most important pathogens in allotransplantation, but the consequences of HCMV cross-species infection of porcine xenografts are unknown. Therefore, we investigated the effects of HCMV infection of porcine endothelial cells (pEC) on cell surface molecule expression and human leukocyte recruitment.

Human leukocyte transmigration across Galalpha(1,3)Gal-negative porcine endothelium is regulated by human CD18 and CD99.

Background: In pig-to-human xenotransplantation cross-species receptor interactions mediate cellular infiltration and rejection of porcine grafts. However, the mechanisms responsible for recruitment of human leukocyte subsets across porcine endothelial cells (EC) remain largely unknown. Here, we investigated the role of CD99, CD18, and Galalpha(1,3)Gal (Gal) in this process.