Institute of Immunology, Faculty of Medicine Comenius University, Bratislava, Slovakia.
National Institute for Tuberculosis, Lung Diseases and Thoracic Surgery, Vysne Hagy, Slovakia.
Mediators Inflamm. 2020 May 14;2020:9501617. doi: 10.1155/2020/9501617. eCollection 2020.
Sarcoidosis and hypersensitivity pneumonitis (HP) are immunologically mediated processes caused by hypersensitivity reaction accompanied by similar features including lymphocytic alveolitis and granuloma formation. Recent studies describe the role of TREM receptors in T cell activation, differentiation, and granuloma formation. Alveolar macrophages activation via TREM receptors may be the key factor mediating subsequent immune response. The aim of the study was to analyse TREM-1 and TREM-2 expression to identify further molecular mechanisms participating in the immunopathogenesis of sarcoidosis and HP.
Flow cytometry was performed to analyse TREM-1 and TREM-2 expression on CD14 cells in bronchoalveolar lavage fluid from patients having sarcoidosis or HP and a control group.
The study proved increased TREM-1 expression on alveolar macrophages in pulmonary sarcoidosis and diminished TREM-1 expression in HP-Sarcoidosis: median: 76.7; HP: median: 29.9; control: median: 53.3, (sarcoidosis versus HP: < 0.001; sarcoidosis versus control: < 0.05). TREM-2 expression was increased in both, sarcoidosis and HP-sarcoidosis: median: 34.79; HP: median: 36.00; control: median: 12.98, (sarcoidosis versus control: < 0.05; HP versus control: < 0.05). Correlation analysis showed negative correlation between TREM-1 and total number of CD8 cytotoxic T cells. In sarcoidosis TREM-1 expression decreased with changes of HRCT image, decrease in CD4/CD8 ratio and decrease in DLCO.
Differences in TREM receptor expression in sarcoidosis (increase in TREM-1 and TREM-2) and HP (increase in TREM-2) and correlation analysis suggests that activation via TREM may participate in typical immunological characteristics of sarcoidosis and HP.
结节病和过敏性肺炎(HP)是由过敏反应引起的免疫介导过程,伴有类似的特征,包括淋巴细胞性肺泡炎和肉芽肿形成。最近的研究描述了 TREM 受体在 T 细胞激活、分化和肉芽肿形成中的作用。通过 TREM 受体激活肺泡巨噬细胞可能是介导随后免疫反应的关键因素。本研究旨在分析 TREM-1 和 TREM-2 的表达,以确定进一步参与结节病和 HP 免疫发病机制的分子机制。
通过流式细胞术分析结节病或 HP 患者和对照组支气管肺泡灌洗液中 CD14 细胞上 TREM-1 和 TREM-2 的表达。
本研究证明,在肺结节病中,肺泡巨噬细胞上的 TREM-1 表达增加,而在 HP-结节病中则减少:中位数:76.7;HP:中位数:29.9;对照组:中位数:53.3(结节病与 HP:<0.001;结节病与对照组:<0.05)。TREM-2 的表达在结节病和 HP-结节病中均增加:中位数:34.79;HP:中位数:36.00;对照组:中位数:12.98(结节病与对照组:<0.05;HP 与对照组:<0.05)。相关性分析显示,TREM-1 与总数量的 CD8 细胞毒性 T 细胞呈负相关。在结节病中,TREM-1 的表达随着 HRCT 图像的变化、CD4/CD8 比值的降低和 DLCO 的降低而降低。
结节病(TREM-1 和 TREM-2 增加)和 HP(TREM-2 增加)中 TREM 受体表达的差异以及相关性分析表明,通过 TREM 的激活可能参与结节病和 HP 的典型免疫学特征。