Mucin expression in peripheral airways of patients with chronic obstructive pulmonary disease
Mucin expression in peripheral airways of patients with chronic obstructive pulmonary disease
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DOI：
10.1111/j.1365-2559.2004.01952.x
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发表时间：
2004-11-01
期刊：
影响因子：
6.4
通讯作者：
Papi, A
中科院分区：
文献类型：
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作者：
Caramori, G;Di Gregorio, C;Papi, A
目的：研究慢性阻塞性肺疾病 (COPD) 患者外周气道中粘蛋白的表达。方法和结果：对患有 COPD 的吸烟者 (n = 9) 和年龄匹配的对照组（包括吸烟者 (n = 11) 和肺功能正常的终身不吸烟者 (n = 6)）的外周肺切片进行阿新蓝、高碘酸希夫 (PAS) 染色和粘蛋白免疫组织化学染色(MUC)：MUC2、MUC4、MUC5AC、MUC5B 和 MUC6。对细支气管上皮的组织化学染色和免疫反应性进行分级，并评估细支气管管腔中是否存在染色粘液。三组之间阿新蓝和PAS上皮染色没有差异。 COPD 受试者中管腔内 PAS 染色的频率明显更高 (P < 0.05)。 COPD患者细支气管上皮中MUC5AC的表达显着升高（P < 0.05）。在细支气管腔内，主要的粘蛋白是MUC5B。 COPD 患者中管腔内 MUC5B 的发生率显着更高（P < 0.05）。结论：COPD 与细支气管管腔中 MUC5B 和细支气管上皮中粘蛋白 MUC5AC 表达增加特异性相关。外周气道粘蛋白产生的这些变化可能有助于慢性阻塞性肺病的病理生理学。
Aims: To study the expression of mucins in peripheral airways in patients with chronic obstructive pulmonary disease (COPD).Methods and results: Peripheral lung sections from smokers with COPD (n = 9) and age-matched controls including smokers (n = 11) and lifelong non-smokers with normal lung function (n = 6) were stained with alcian blue, periodic acid-Schiff (PAS) and by immunohistochemistry of mucins (MUC): MUC2, MUC4, MUC5AC, MUC5B and MUC6. Histochemical staining and immunoreactivity of bronchiolar epithelium were graded and the presence or absence of stained mucus in the bronchiolar lumen was evaluated. There were no differences in alcian blue and PAS epithelial staining between the three groups. Intraluminal PAS staining was significantly more frequent among COPD subjects (P < 0.05). The expression of MUC5AC was significantly higher in the bronchiolar epithelium of patients with COPD (P < 0.05). Within the bronchiolar lumen, the predominant mucin was MUC5B. Intraluminal MUC5B was significantly more frequent among COPD patients (P < 0.05).Conclusions: COPD is specifically associated with increased expression of MUC5B in the bronchiolar lumen and of the mucin MUC5AC in the bronchiolar epithelium. These changes in mucin production in the peripheral airways may contribute to the pathophysiology of COPD.