Altered serum levels of type I collagen turnover indicators accompanied by IL-6 and IL-8 release in stable COPD
Altered serum levels of type I collagen turnover indicators accompanied by IL-6 and IL-8 release in stable COPD
复制标题
稳定期 COPD 患者血清 I 型胶原蛋白周转指标水平发生改变,并伴有 IL-6 和 IL-8 释放
DOI:
10.2147/copd.s188139
复制
发表时间:
2019-01-01
影响因子:
2.8
通讯作者:
Zhang, Jing
中科院分区:
文献类型:
--
作者:
Zeng, Ying-Ying;Hu, Wei-Ping;Zhang, Jing
Background COPD, characterized by chronic inflammation and airway remodeling, has significant pathological alterations in composition and deposition of the extracellular matrix. The expression of procollagen 1 C-terminal peptide (PICP) and collagen type 1 C-terminal telopeptide (ICTP), two major by-products in the synthesis and degradation of collagen, was shown to be positively correlated with inflammatory mediator levels in previous studies. Purpose In this study, we investigated whether the serum concentrations of PICP and ICTP were associated with the inflammation level for patients with stable COPD. Patients and methods We collected serum samples from 25 control subjects and 20 patients with stable COPD from December 2011 to October 2012 in Shanghai Zhongshan Hospital and Shanghai Dahua Hospital. We determined concentrations of PICP, ICTP, C-reactive protein (CRP), IL-6, IL-8, and tumor necrosis factor (TNF)-α by using enzyme-linked immunosorbent assay methods. Results Demographic characteristics were comparable between the two groups. In patients with stable COPD, serum levels of CRP, IL-6, IL-8, and TNF-α were all elevated compared to control subjects, but only changes of IL-6 achieved statistical significance. Serum concentration of PICP was significantly elevated in patients with COPD, and level of ICTP was slightly decreased. Moreover, serum concentrations of PICP were positively correlated with the levels of both IL-6 and IL-8. Conclusion The increased levels of serum PICP in COPD might indicate the condition of airway remodeling, and IL-6 and/or IL-8 might play an important role in stimulating collagen synthesis.