Centre for Respiratory Health, School of Medicine & Pharmacology, University of Western Australia, Perth, WA, Australia; Stem Cell Unit, Institute for Respiratory Health, Perth, WA, Australia.
Centre for Respiratory Health, School of Medicine & Pharmacology, University of Western Australia, Perth, WA, Australia; Stem Cell Unit, Institute for Respiratory Health, Perth, WA, Australia.
Respir Med. 2017 Nov;132:261-264. doi: 10.1016/j.rmed.2017.04.014. Epub 2017 Apr 26.
Chronic obstructive pulmonary disease (COPD) is characterized by progressive pulmonary and systemic inflammation. Acute exacerbations of COPD (AECOPD) are associated with acute inflammation and infections and increase the rates of morbidity and mortality. Currently, neither the aetiology nor pathogenesis of AECOPD are entirely understood. Exosomes have been reported to regulate immunity and inflammation via specific intercellular communications through an array of macromolecules (e.g. microRNA and proteins) contained within these microvesicles. We evaluated the level of circulating exosomes in relation to systemic inflammation in patients with AECOPD (n = 20) or stable COPD (sCOPD; n = 20) in comparison to non-smoking healthy controls (n = 20). Exosomes in plasma were isolated by precipitation-based method, and quantified using a CD9 expression based enzyme-linked immunosorbent assay (ELISA). Plasma biomarkers of systemic inflammation, C-reactive protein (CRP), soluble tumour necrosis factor receptor-1 (sTNFR1) and interleukin (IL)-6 were also quantified using ELISA. Levels of plasma exosome were higher in AECOPD patients (p < 0.001) and sCOPD patients (p < 0.05) compared to controls. Plasma levels of CRP and sTNFR1 were highest in AECOPD, followed by sCOPD patients compared to healthy controls (p < 0.05). Plasma IL-6 was elevated in AECOPD (p < 0.05) and sCOPD patients (p < 0.01) compared to controls. The level of exosome correlated with the levels of CRP, sTNFR1 and IL-6 in plasma. Exosomes may therefore be involved in the inflammatory process of AECOPD. Further studies involving exosomal phenotyping and molecular characterization are required to fully understand their role in the pathophysiology of COPD.
慢性阻塞性肺疾病(COPD)的特征是肺部和全身炎症的进行性发展。COPD 急性加重(AECOPD)与急性炎症和感染有关,并增加发病率和死亡率。目前,AECOPD 的病因和发病机制尚不完全清楚。已经有报道称,外泌体通过含有这些微泡的一系列大分子(如 microRNA 和蛋白质)进行特定的细胞间通讯,从而调节免疫和炎症。我们评估了与 AECOPD(n=20)或稳定期 COPD(sCOPD;n=20)患者全身炎症相关的循环外泌体水平,并与不吸烟的健康对照者(n=20)进行了比较。通过沉淀法分离血浆中外泌体,并使用基于 CD9 表达的酶联免疫吸附测定法(ELISA)进行定量。还使用 ELISA 定量测定了血浆生物标志物全身炎症的 C 反应蛋白(CRP)、可溶性肿瘤坏死因子受体-1(sTNFR1)和白细胞介素(IL)-6。与对照组相比,AECOPD 患者(p<0.001)和 sCOPD 患者(p<0.05)的血浆外泌体水平更高。AECOPD 患者的 CRP 和 sTNFR1 血浆水平最高,其次是 sCOPD 患者,与健康对照组相比(p<0.05)。AECOPD 患者(p<0.05)和 sCOPD 患者(p<0.01)的血浆 IL-6 水平升高与对照组相比。外泌体水平与 CRP、sTNFR1 和 IL-6 水平在血浆中呈正相关。因此,外泌体可能参与 AECOPD 的炎症过程。需要进一步进行外泌体表型和分子特征的研究,以充分了解它们在 COPD 病理生理学中的作用。