Lemström K, Kallio E, Krebs R, Bruggeman C, Häyry P, Koskinen P
Transplantation Laboratory, University of Helsinki, Finland.
Transpl Int. 1996;9 Suppl 1:S221-2. doi: 10.1007/978-3-662-00818-8_56.
A cascade of inflammation and injury of the airway wall followed by a fibroproliferative process that results in airway obstruction has been suggested as the explanation of the process of obliterative bronchiolitis (OB) in lung allograft recipients. To determine the impact of rat cytomegalovirus (RCMV) infection on the development of OB, heterotopic rat tracheal allografts were transplanted from DA donors to WF recipients immunosuppressed with 2 mg/kg per day cyclosporine A. Chronic RCMV infection was similarly established 8 weeks before transplantation in donors alone (D+/R-), recipients alone (D-/R+), and both donors and recipients (D+/R+). The control rats were left non-infected, but were similarly immunosuppressed. The results of this study demonstrate that both acute and chronic recipient RCMV infection, but not donor infection, amplify the development of experimental OB in the rat and suggest that RCMV infection-associated immune response, rather than the viral load in the graft, is essential for the development of the accelerated form of OB.
