Coll-Vinent B, Cebrián M, Cid M C, Font C, Esparza J, Juan M, Yagüe J, Urbano-Márquez A, Grau J M
University of Barcelona, Spain.
Arthritis Rheum. 1998 Mar;41(3):435-44. doi: 10.1002/1529-0131(199803)41:3<435::AID-ART9>3.0.CO;2-9.
To investigate endothelial cell adhesion molecule expression in vessels from patients with classic polyarteritis nodosa (PAN).
Frozen sections of 21 muscle and 16 nerve samples from 30 patients with biopsy-proven PAN and 12 histologically normal muscle and 2 histologically normal nerve samples from 12 controls were studied immunohistochemically, using specific monoclonal antibodies (MAb) that recognize adhesion molecules. Adhesion molecules identified were intercellular adhesion molecule 1 (ICAM-1), ICAM-2, ICAM-3, vascular cell adhesion molecule 1 (VCAM-1), platelet endothelial cell adhesion molecule 1 (PECAM-1), E-selectin, P-selectin, L-selectin, lymphocyte function-associated antigen 1 (LFA-1), and very late activation antigen 4 (VLA-4). Neutrophils were identified with a MAb recognizing neutrophil elastase. Endothelial cells were identified with the lectin ulex europaeus.
In early lesions, expression of PECAM-1, ICAM-1, ICAM-2, and P-selectin was similar to that in control samples, and VCAM-1 and E-selectin were induced in vascular endothelium. In advanced lesions, immunostaining for adhesion molecules diminished or disappeared in luminal endothelium, whereas these molecules were clearly expressed in microvessels within and surrounding inflamed vessels. Staining in endothelia from vessels in a healing stage tended to be negative. A high proportion of infiltrating leukocytes expressed LFA-1 and VLA-4, and only a minority expressed L-selectin. No relationship between the expression pattern of adhesion molecules and clinical features, disease duration, or previous corticosteroid treatment was observed.
Endothelial adhesion molecule expression in PAN is a dynamic process that varies according to the histopathologic stage of the vascular lesions. The preferential expression of constitutive and inducible adhesion molecules in microvessels suggests that angiogenesis contributes to the persistence of inflammatory infiltration in PAN.
研究结节性多动脉炎（PAN）患者血管中内皮细胞粘附分子的表达情况。
对30例经活检证实为PAN患者的21份肌肉和16份神经样本的冰冻切片，以及12例对照者的12份组织学正常肌肉和2份组织学正常神经样本的冰冻切片进行免疫组织化学研究，使用识别粘附分子的特异性单克隆抗体（MAb）。所鉴定的粘附分子包括细胞间粘附分子1（ICAM-1）、ICAM-2、ICAM-3、血管细胞粘附分子1（VCAM-1）、血小板内皮细胞粘附分子1（PECAM-1）、E-选择素、P-选择素、L-选择素、淋巴细胞功能相关抗原1（LFA-1）和极晚期活化抗原4（VLA-4）。用识别中性粒细胞弹性蛋白酶的MAb鉴定中性粒细胞。用荆豆凝集素鉴定内皮细胞。
在早期病变中，PECAM-1、ICAM-1、ICAM-2和P-选择素的表达与对照样本相似，而VCAM-1和E-选择素在血管内皮中被诱导表达。在晚期病变中，管腔内皮层中粘附分子的免疫染色减弱或消失，而这些分子在炎症血管内及周围的微血管中明显表达。愈合期血管内皮的染色往往为阴性。高比例的浸润白细胞表达LFA-1和VLA-4，只有少数表达L-选择素。未观察到粘附分子表达模式与临床特征、疾病持续时间或先前皮质类固醇治疗之间存在关联。
PAN中内皮粘附分子的表达是一个动态过程，根据血管病变的组织病理学阶段而变化。组成型和诱导型粘附分子在微血管中的优先表达表明血管生成有助于PAN中炎症浸润的持续存在。
