背景:慢性阻塞性肺疾病(COPD)是一种复杂的慢性炎症性疾病。研究COPD急性加重的特点对制定新的治疗策略具有重要意义。
目的:本研究旨在确定人β-防御素-2(hBD-2)水平与COPD加重之间的关系。
方法:我们检测了来自广州的254例患者的痰液hBD-2水平,中国,2年。研究参与者分为COPD组(n=203,GOLD0-4)和对照组(n=51,40-79岁)。在基线,第十二个月,第24个月,我们检测痰液hBD-2水平和细胞因子水平,如CXCL10、CXCL11和IFN。
结果:在基线时,患者和对照组之间的痰液和血清hBD-2水平没有显着差异。然而,在接下来的2年内至少有一种症状加重的患者的痰hBD-2水平显着低于没有任何恶化的患者(1130.9±858.4pg/mLvs.2103.7±1294.2pg/mL,分别为;p=0.001)。然而,患者(无加重史)和对照组之间痰液hBD-2水平无统计学差异(2084.9±1317.6pg/mLvs.2152.5±1251.6pg/mL,分别为;p=0.626)。我们使用逻辑回归模型来评估加重与痰hBD-2水平之间的关系。有趣的是,我们发现低hBD-2水平(<1000pg/mL)与急性加重显著相关.具体来说,hBD-2水平较低的患者在接下来的12个月内更有可能出现恶化(0.333vs.0.117;p=0.001)。此外,我们比较了对照组和GOLD3-4患者的hBD-2水平,发现细菌(+)和/或病毒(+)参与者的hBD-2水平与疾病严重程度相关(p=0.02).
结论:有恶化风险的患者更可能有较低的痰hBD-2水平。这些结果对COPD的未来治疗具有重要意义。
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a complicated chronic inflammatory disease. It is important to investigate the characteristics of acute exacerbation of COPD to develop new therapeutic strategies.
OBJECTIVE: This study aimed to determine the relationship between the human beta-defensin-2 (hBD-2) levels and aggravation of COPD.
METHODS: We detected the sputum hBD-2 level of 254 patients from Guangzhou,
China, for 2 years. The study participants were categorized into the COPD group (n = 203, GOLD 0-4) and the control group (n = 51, 40-79 years old). At baseline, 12th month, and 24th month, we detected the sputum hBD-2 level and levels of cytokines, such as CXCL10, CXCL11, and IFN.
RESULTS: At baseline, there were no significant differences in the sputum and serum hBD-2 levels between the patients and the controls. However, the sputum hBD-2 levels of patients who had at least one symptom aggravation over the next 2 years were significantly lower than those of patients without any
exacerbations (1130.9 ± 858.4 pg/mL vs. 2103.7 ± 1294.2 pg/mL, respectively; p = 0.001). Nevertheless, there were no statistically significant differences in the sputum hBD-2 levels between patients (no aggravation history) and controls (2084.9 ± 1317.6 pg/mL vs. 2152.5 ± 1251.6 pg/mL, respectively; p = 0.626). We used a logistic regression model to assess the relationship between aggravation and sputum hBD-2 levels. Interestingly, we found that low hBD-2 level (< 1000 pg/mL) was significantly associated with
exacerbations. Specifically, patients with low hBD-2 levels were more likely to experience
exacerbations in the next 12 months (0.333 vs. 0.117; p = 0.001). Moreover, we compared the hBD-2 levels between controls and patients with GOLD 3-4 and found that participants with bacteria (+) and/or viruses (+) had an association between hBD-2 level and disease severity (p = 0.02).
CONCLUSIONS: Patients at risk of
exacerbations are more likely to have lower sputum hBD-2 levels. These results have important implications for future therapies for COPD.