Steinhoff G, You X M, Steinmüller C, Boeke K, Stals F S, Bruggeman C A, Haverich A
Department of Cardiovascular Surgery, University of Kiel, Germany.
Scand J Infect Dis Suppl. 1995;99:58-60.
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.
巨细胞病毒（CMV）感染是心脏和肺移植中慢性移植排斥反应发生的主要危险因素。CMV感染诱发肺移植排斥反应的一种可能机制是病毒感染导致黏附配体分子的炎症上调，进而增加内皮细胞与白细胞的相互作用。为研究这一问题，利用大鼠巨细胞病毒（RCMV）感染和左单肺移植中的急性肺移植排斥反应，在大鼠中建立了一个实验模型。通过免疫组织化学研究了RCMV、细胞间黏附分子-1（ICAM-1）及其白细胞受体CD11a（LFA-1）的分布。早在第11天就在受感染宿主的移植肺中观察到病毒感染。RCMV感染诱导并增强了内皮细胞上ICAM-1的表达，且发现受感染受体中CD11a阳性白细胞的浸润增加。发现宿主对同种异体移植物的排斥反应加速。
