Jiang Z, Woda B A, Savas L, Fraire A E
Department of Pathology, University of Massachusetts Medical School, Worcester, USA.
Mod Pathol. 1998 Dec;11(12):1189-92.
Intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), and the lymphocyte function-associated antigen (LFA-1) are cell adhesion molecules thought to play an important role in the complex process of airway inflammation and tumor cell growth. The aim of this study was to examine the distribution of ICAM-1, VCAM-1, and LFA-1 in adenocarcinoma of lung and in major cellular compartments of non-neoplastic lung tissue. We examined cellular compartments in tissue from five bronchoalveolar carcinomas, three acinar adenocarcinomas, and one colon cancer metastatic to the lung. The compartments in neoplasms included the tumor cells proper, endothelial cells within the tumor vasculature, tumor stromal cells, and tumor-infiltrating lymphocytes. The compartments in non-neoplastic lung tissue included lung endothelial cells, pulmonary lymphocytes, interstitial fibroblasts, Type II alveolar pneumocytes, and bronchial epithelial cells. ICAM-1 was expressed in tumor cells from all of the nine adenocarcinomas. In contrast, VCAM-1 expression was not identified in tumor cells from any of the nine adenocarcinomas. ICAM-1 was expressed in all cellular compartments of the non-neoplastic lung tissue, whereas VCAM-1 was expressed only in pulmonary lymphocytes and interstitial fibroblastic cells. LFA-1 was uniformly expressed in tumor-infiltrating lymphocytes from each of the nine tumors and all of the lymphocytes in non-neoplastic lung tissue. This study showed major differences in the expression of ICAM-1 and VCAM-1 in tumor cells from pulmonary adenocarcinoma and also provided evidence for a wider distribution of ICAM-1, compared with VCAM-1, in non-neoplastic cellular compartments of the lung. ICAM-1 expression was particularly noticeable in bronchial and alveolar epithelial cells. Upregulation of ICAM-1 in pulmonary adenocarcinoma might foster binding by LFA-1-bearing lymphocytes, with a possible impact on the vulnerability of tumor cells to host defense mechanisms.
细胞间黏附分子（ICAM-1）、血管细胞黏附分子（VCAM-1）和淋巴细胞功能相关抗原（LFA-1）是细胞黏附分子，被认为在气道炎症和肿瘤细胞生长的复杂过程中起重要作用。本研究的目的是检测ICAM-1、VCAM-1和LFA-1在肺腺癌以及非肿瘤性肺组织主要细胞成分中的分布。我们检测了5例细支气管肺泡癌、3例腺泡腺癌和1例肺转移结肠癌组织中的细胞成分。肿瘤中的细胞成分包括肿瘤细胞本身、肿瘤脉管系统内的内皮细胞、肿瘤基质细胞和肿瘤浸润淋巴细胞。非肿瘤性肺组织中的细胞成分包括肺内皮细胞、肺淋巴细胞、间质成纤维细胞、II型肺泡上皮细胞和支气管上皮细胞。9例腺癌的肿瘤细胞均表达ICAM-1。相比之下，9例腺癌的肿瘤细胞中均未检测到VCAM-1表达。ICAM-1在非肿瘤性肺组织的所有细胞成分中均有表达，而VCAM-1仅在肺淋巴细胞和间质成纤维细胞中表达。LFA-1在9例肿瘤中的肿瘤浸润淋巴细胞以及非肿瘤性肺组织中的所有淋巴细胞中均呈均匀表达。本研究显示了肺腺癌肿瘤细胞中ICAM-1和VCAM-1表达的主要差异，同时也提供了证据表明，与VCAM-1相比，ICAM-1在肺非肿瘤性细胞成分中的分布更广。ICAM-1在支气管和肺泡上皮细胞中的表达尤为明显。肺腺癌中ICAM-1的上调可能促进携带LFA-1的淋巴细胞的黏附，这可能会影响肿瘤细胞对宿主防御机制的易感性。
