Induction of endothelial adhesion molecules by rat cytomegalovirus in allogeneic lung transplantation in the rat.

Cytomegalovirus (CMV) infection is known to be a major risk factor for the development of chronic transplant rejection in heart and lung transplantation. A possible mechanism for the induction of lung transplant rejection by CMV infection is the inflammatory upregulation of adhesion ligand molecules by the viral infection leading to an increased endothelial-leucocyte interaction. To study this question, an experimental model was established in the rat using a rat cytomegalovirus (RCMV) infection and acute lung transplant rejection in left single lung transplantation. The distribution of RCMV, intercellular adhesion molecule-1 (ICAM-1) and its leucocyte receptor CD11a (LFA-1) were investigated by immunohistochemistry. The viral infection was observed in transplant lungs of infected hosts as early as day 11. The expression of ICAM-1 on endothelial cells was induced and enhanced by RCMV infection, and infiltration of CD11a-positive leucocytes found to be increased in infected recipients. An acceleration of the rejection of the allografts by the hosts was found.