Association of innate defense proteins BPIFA1 and BPIFB1 with disease severity in COPD.

Association of innate defense proteins BPIFA1 and BPIFB1 with disease severity in COPD.
复制标题

DOI:
10.2147/copd.s144136
复制
发表时间:
2018
影响因子:
2.8
通讯作者:
Bracke KR
Bracke KR
中科院分区:
医学3区
文献类型:
--
作者:
De Smet EG;Seys LJ;Verhamme FM;Vanaudenaerde BM;Brusselle GG;Bingle CD;Bracke KR

文献摘要

被引文献

相似文献

慢性阻塞性肺病(COPD)的特点是吸入有毒颗粒和气体引起的肺部异常炎症反应。气道上皮通过维持物理屏障和分泌防御蛋白(例如杀菌/通透性增加倍数 (BPIF) 蛋白、BPIFA1 和 BPIFB1),对这些有害物质具有保护功能。然而,迄今为止,关于吸烟者和 COPD 患者中 BPIFA1 表达的数据不一致。因此,我们研究了一大群从不吸烟者和患有或不患有慢性阻塞性肺病的吸烟者中 BPIFA1 和 BPIFB1 的表达,包括肺组织中的信使 RNA (mRNA) 水平和气道上皮中的蛋白质水平。此外,我们检查了 BPIFA1 和 BPIFB1 水平、杯状细胞增生和肺功能测量之间的相关性。与 II 期 COPD 患者和无 COPD 受试者相比,III-IV 期 COPD 患者中 BPIFA1 和 BPIFB1 mRNA 表达显着增加。此外,与没有慢性阻塞性肺病的受试者相比,慢性阻塞性肺病患者的蛋白质水平显着增加。 BPIFA1 和 BPIFB1 水平与气流受限的测量值呈负相关,与杯状细胞增生呈正相关。此外,通过免疫荧光双染,我们证明了BPIFB1在杯状细胞中的表达。总之,我们表明 BPIFA1 和 BPIFB1 水平在 COPD 患者中升高,并且与疾病严重程度相关。
Chronic obstructive pulmonary disease (COPD) is characterized by an abnormal inflammatory response in the lungs caused by the inhalation of noxious particles and gases. The airway epithelium has a protective function against these harmful agents by maintaining a physical barrier and by secreting defensive proteins, such as bactericidal/permeability-increasing fold-containing (BPIF) proteins, BPIFA1 and BPIFB1. However, inconsistent data regarding BPIFA1 expression in smokers and COPD patients have been reported to date. Therefore, we investigated the expression of BPIFA1 and BPIFB1 in a large cohort of never-smokers and smokers with and without COPD, both on the messenger RNA (mRNA) level in lung tissue and on the protein level in airway epithelium. Furthermore, we examined the correlation between BPIFA1 and BPIFB1 levels, goblet cell hyperplasia, and lung function measurements. BPIFA1 and BPIFB1 mRNA expressions were significantly increased in stage III–IV COPD patients compared with stage II COPD patients and subjects without COPD. In addition, protein levels in COPD patients were significantly increased in comparison with subjects without COPD. BPIFA1 and BPIFB1 levels were inversely correlated with measurements of airflow limitation and positively correlated with goblet cell hyperplasia. In addition, by the use of immunofluorescence double staining, we demonstrated the expression of BPIFB1 in goblet cells. In conclusion, we show that BPIFA1 and BPIFB1 levels are elevated in COPD patients and correlate with disease severity.