Southcott A M, Hemingway I, Lorimer S, Sugars K, Hellewell P G, Black C M, Jeffery P K, Gearing A J, Haskard D O, du Bois R M
Interstitial Lung Disease Unit, Royal Brompton Hospital, London, UK.
Eur Respir J. 1998 Jan;11(1):91-8. doi: 10.1183/09031936.98.11010091.
Cellular adhesion molecules are crucial determinants of the migration of immune effector cells to the tissues. In chronic inflammatory diseases, upregulation of the expression of these molecules may contribute to the persistent inflammatory process. The aim of this study was to determine whether there is evidence of adhesion molecule expression in chronically inflamed lung. Soluble adhesion molecules in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunoassay in 54 patients with chronic interstitial lung diseases and 16 normal controls. Adhesion molecule expression in fibrosing alveolitis (FA) lung and in control lung was assessed using immunohistology and reverse transcription-polymerase chain reaction (RT-PCR) amplification. Soluble intercellular adhesion molecule-1 (ICAM-1) was detected in all but two subjects. There was no difference in ICAM-1 concentration between disease groups and normal subjects. In contrast, soluble E-selectin was detected in 17 of the 70 subjects and was significantly associated with the presence of lung disease (p=0.0173). Furthermore, the presence of soluble E-selectin was associated with a raised lymphocyte percentage in BALF (p=0.0069). Soluble VCAM was only detected in five of the 70 subjects (two normals, three patients). There was no difference in adhesion molecule expression in lung parenchyma between FA and controls assessed by immunohistology and RT-PCR. The most striking finding of our study was the universal expression of intercellular adhesion molecule-1 in both normal and diseased lung, emphasizing the important role of the lung in immune function. Upregulation of E-selectin may contribute to inflammatory cell accumulation in chronic interstitial lung diseases.
细胞黏附分子是免疫效应细胞向组织迁移的关键决定因素。在慢性炎症性疾病中,这些分子表达的上调可能会导致持续性炎症过程。本研究的目的是确定在慢性炎症的肺组织中是否存在黏附分子表达的证据。采用酶联免疫吸附测定法检测了54例慢性间质性肺疾病患者和16例正常对照者支气管肺泡灌洗液(BALF)中的可溶性黏附分子。使用免疫组织学和逆转录-聚合酶链反应(RT-PCR)扩增评估了肺纤维化(FA)患者肺组织和对照肺组织中黏附分子的表达。除两名受试者外,所有受试者均检测到可溶性细胞间黏附分子-1(ICAM-1)。疾病组和正常受试者之间的ICAM-1浓度没有差异。相比之下,在70名受试者中有17名检测到可溶性E-选择素,且其与肺部疾病的存在显著相关(p = 0.0173)。此外,可溶性E-选择素的存在与BALF中淋巴细胞百分比升高相关(p = 0.0069)。可溶性血管细胞黏附分子(VCAM)仅在70名受试者中的5名(2名正常受试者,3名患者)中检测到。通过免疫组织学和RT-PCR评估,FA患者和对照者肺实质中黏附分子的表达没有差异。我们研究中最显著的发现是细胞间黏附分子-1在正常肺组织和患病肺组织中均普遍表达,这强调了肺在免疫功能中的重要作用。E-选择素的上调可能有助于慢性间质性肺疾病中炎症细胞的积聚。