Kim Won-Dong, Chi Hyun-Sook, Choe Kang-Hyeon, Kim Woo-Sung, Hogg James C, Sin Don D
Department of Pulmonary and Critical Care Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Department of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Tuberc Respir Dis (Seoul). 2020 Dec;83(Supple 1):S25-S33. doi: 10.4046/trd.2020.0089. Epub 2020 Oct 20.
Lung inflammation plays a vital role in the pathogenesis of chronic obstructive pulmonary disease (COPD), but the characteristics of the inflammatory process remain unclear. There is growing interest in the role of granzyme B (GzmB) because CD8+ T cells can induce apoptosis of target cells by releasing GzmB, which in turn may cause tissue injury and remodeling. However, GzmB is also expressed by regulatory cells, which are able to suppress CD8+ T cell. The role of GzmB+ cells needs to be defined in COPD.
GzmB+ and CD8+ cells on alveolar wall of surgically resected lungs of microscopically classified 12 nonsmoking control, 12 panlobular emphysema (PLE) and 30 centrilobular emphysema (CLE) subjects were localized by immunohistochemical method. Positively stained cells on alveolar wall were counted and length of corresponding alveolar wall was measured. The results were expressed as mean number of positively stained cells per mm of alveolar wall in each subject.
The number of GzmB+ and CD8+ cells on alveolar wall of CLE was greater than that of control or PLE subjects (p<0.05 and p<0.001, respectively). There was a positive relationship between the number of alveolar GzmB+ cells and forced expiratory volume in 1 second (FEV1) (r=0.610, p=0.003) in CLE subjects. The number of alveolar GzmB+ cells progressively decreased with decline of FEV1.
Our finding that number of alveolar GzmB+ cells was associated with FEV1 suggests that GzmB+ cells might have protective role in the progression of lung destruction and airflow limitation in CLE, which is the predominant emphysema subtype of COPD.
肺部炎症在慢性阻塞性肺疾病(COPD)的发病机制中起着至关重要的作用,但炎症过程的特征仍不清楚。由于CD8 + T细胞可通过释放颗粒酶B(GzmB)诱导靶细胞凋亡,进而可能导致组织损伤和重塑,因此人们对GzmB的作用越来越感兴趣。然而,GzmB也由调节细胞表达,调节细胞能够抑制CD8 + T细胞。在COPD中,GzmB +细胞的作用需要明确。
采用免疫组织化学方法对12例显微镜分类的非吸烟对照者、12例全小叶型肺气肿(PLE)患者和30例小叶中心型肺气肿(CLE)患者手术切除肺的肺泡壁上的GzmB +和CD8 +细胞进行定位。计数肺泡壁上的阳性染色细胞,并测量相应肺泡壁的长度。结果以每个受试者每毫米肺泡壁上阳性染色细胞的平均数表示。
CLE患者肺泡壁上GzmB +和CD8 +细胞的数量多于对照组或PLE患者(分别为p < 0.05和p < 0.001)。在CLE患者中,肺泡GzmB +细胞数量与一秒用力呼气容积(FEV1)之间存在正相关(r = 0.610,p = 0.003)。随着FEV1下降,肺泡GzmB +细胞数量逐渐减少。
我们发现肺泡GzmB +细胞数量与FEV1相关,这表明GzmB +细胞可能在CLE(COPD的主要肺气肿亚型)的肺破坏和气流受限进展中起保护作用。