Sansonno D, Cornacchiulo V, Gatti P, Dammacco F
Department of Biomedical Sciences and Human Oncology, University of Bari Medical School, Italy.
Int J Clin Lab Res. 1992;22(2):100-5. doi: 10.1007/BF02591405.
Intercellular adhesion molecule-1, an immunoglobulin supergene family member, is known to account for important steps in cell activation and the immune response. By a non-isotopic slot-dot immunoblotting assay, we measured circulating levels of intercellular adhesion molecule-1 in 26 patients with hepatitis C virus-associated chronic active liver disease before and after beta-interferon therapy, in 6 patients with non-A, non-B acute self-limiting hepatitis and in 13 healthy subjects. Circulating intercellular adhesion molecule-1 was found in 10 of 13 (77%) normal controls at low concentrations which were not statistically different from those measured in patients with hepatitis C virus-associated chronic active liver disease responsive to beta-interferon, whereas significantly higher levels were found in unresponsive patients. Higher serum intercellular adhesion molecule-1 levels were found in 4 of 10 (40%) beta-interferon-responsive patients compared with 13 of 16 (18%) unresponsive patients. Intercellular adhesion molecule-1 levels persisted after discontinuation of beta-interferon treatment and did not correlate with hepatocytolysis (as indicated by alanine aminotransferase serum activity) either in chronic active liver disease or acute hepatitis. However, a good correlation was found between intercellular adhesion molecule-1 and its expression on liver cells, thus emphasizing that induced circulating levels may reflect the state of activation at the sites of the inflammatory process. These data strongly support the view that intercellular adhesion molecule-1 plays an important role in liver cell damage in hepatitis C virus-associated acute and chronic liver disease, and that its circulating levels may be a good prognostic parameter of responsiveness to beta-interferon therapy.
细胞间黏附分子-1是免疫球蛋白超基因家族的一员，已知其在细胞活化和免疫反应中起着重要作用。我们采用非同位素斑点免疫印迹法，检测了26例丙型肝炎病毒相关性慢性活动性肝病患者在β-干扰素治疗前后、6例非甲非乙型急性自限性肝炎患者以及13名健康受试者体内循环中的细胞间黏附分子-1水平。在13名正常对照者中，有10名（77%）检测到低浓度的循环细胞间黏附分子-1，其浓度与对β-干扰素治疗有反应的丙型肝炎病毒相关性慢性活动性肝病患者所测浓度无统计学差异，而在无反应的患者中发现其水平显著更高。与16名无反应患者中的13名（18%）相比，10名对β-干扰素治疗有反应的患者中有4名（40%）血清细胞间黏附分子-1水平更高。在β-干扰素治疗停止后，细胞间黏附分子-1水平持续存在，且在慢性活动性肝病或急性肝炎中均与肝细胞溶解（以丙氨酸转氨酶血清活性表示）无关。然而，发现细胞间黏附分子-1与其在肝细胞上的表达之间有良好的相关性，从而强调诱导的循环水平可能反映炎症过程部位的活化状态。这些数据有力地支持了这样一种观点，即细胞间黏附分子-1在丙型肝炎病毒相关性急慢性肝病的肝细胞损伤中起重要作用，其循环水平可能是对β-干扰素治疗反应性的一个良好预后参数。
