Lautenschlager I T, Höckerstedt K A
Transplantation Laboratory, University of Helsinki, Finland.
Transplantation. 1993 Dec;56(6):1495-9. doi: 10.1097/00007890-199312000-00041.
Intercellular adhesion molecule-1 (ICAM-1) induction on hepatocytes was investigated in relation to acute liver allograft rejection, CMV infection, and systemic bacterial infections. Twenty-four liver transplant recipients underwent an episode of acute rejection, 13 developed a symptomatic clinical CMV infection, and 7 had bacterial sepsis. Seven recipients without rejection or infection complications were used as controls. All rejection episodes monitored by frequent FNABs were reversible, and lymphocyte and lymphoid blast-dominated with a with peak of inflammation (7.2 +/- 3.9 corrected increment units [CIU]). The rejections were treated with high-dose steroids, and the inflammation subsided within one week. ICAM-1 was demonstrated from fine needle aspiration biopsy (FNAB) preparations by a monoclonal antibody and immunoperoxidase staining. ICAM-1 was not detected on the hepatocytes immediately after transplantation or in control patients, but was always seen during rejection. ICAM-1 appeared 1-5 days before the onset of inflammation in FNAB. The intensity of ICAM-1 expression increased toward the peak of inflammation and subsided together with inflammation. During CMV infection a mild immune activation was seen in FNAB (peak 2.5 +/- 0.8 CIU) and in blood. An intense ICAM-1 induction also preceded the immune activation caused by CMV, and subsided slowly with successful antiviral treatment. In addition, a slight ICAM-1 induction on the hepatocytes was recorded during bacterial sepsis. ICAM-1 induction on hepatocytes appears to be linked with an early phase of immune response, and it even precedes the lymphoid activation of rejection. However, several infections, such as CMV and bacterial infections, raise an immune response and may also induce ICAM-1. In conclusion, ICAM-1 induction on hepatocytes can be considered an early, though unspecific, marker for acute liver allograft rejection.
研究了肝细胞上细胞间粘附分子-1（ICAM-1）的诱导与急性肝移植排斥反应、巨细胞病毒（CMV）感染和全身性细菌感染的关系。24例肝移植受者经历了急性排斥反应，13例发生了有症状的临床CMV感染，7例发生了细菌性败血症。7例无排斥反应或感染并发症的受者作为对照。通过频繁的细针穿刺抽吸活检（FNAB）监测的所有排斥反应均为可逆性，淋巴细胞和淋巴母细胞为主，炎症高峰时（校正增量单位[CIU]为7.2±3.9）。排斥反应采用大剂量类固醇治疗，炎症在一周内消退。通过单克隆抗体和免疫过氧化物酶染色从细针穿刺活检（FNAB）标本中检测到ICAM-1。移植后立即在肝细胞上未检测到ICAM-1，对照患者中也未检测到，但在排斥反应期间总是可以看到。ICAM-1在FNAB中炎症发作前1-5天出现。ICAM-1表达强度随着炎症高峰而增加，并与炎症一起消退。在CMV感染期间，FNAB（峰值2.5±0.8 CIU）和血液中出现轻度免疫激活。CMV引起的免疫激活之前也有强烈的ICAM-1诱导，随着抗病毒治疗成功而缓慢消退。此外，在细菌性败血症期间，肝细胞上记录到轻微的ICAM-1诱导。肝细胞上ICAM-1的诱导似乎与免疫反应的早期阶段有关，甚至在排斥反应的淋巴细胞激活之前。然而，一些感染，如CMV和细菌感染，会引发免疫反应，也可能诱导ICAM-1。总之，肝细胞上ICAM-1的诱导可被视为急性肝移植排斥反应的一个早期但非特异性的标志物。
