Disease-specific dynamic biomarkers selected by integrating inflammatory mediators with clinical informatics in ARDS patients with severe pneumonia.
Disease-specific dynamic biomarkers selected by integrating inflammatory mediators with clinical informatics in ARDS patients with severe pneumonia.
复制标题
将炎症介质与重症肺炎 ARDS 患者临床信息相结合，选择疾病特异性动态生物标志物
DOI：
10.1007/s10565-016-9322-4
复制
发表时间：
2016-06
影响因子：
6.1
通讯作者：
Yang S
中科院分区：
文献类型：
--
作者：
Chen C;Shi L;Li Y;Wang X;Yang S
急性呼吸窘迫综合征（ARDS）是一种异质综合征，由于各种危险因素（包括直接或间接的肺损伤）以及严重的肺炎（SP）引起的全身性炎症。由于缺乏疾病特异性的生物标志物，与SP征收的发病率和死亡率保持较高。本研究旨在通过将炎症介质的蛋白质组学特征与临床信息学整合到SP或SP-dard中的疾病特异性生物标志物。 Plasma was sampled from the healthy as controls or patients with SP infected with bacteria or infection-associated SP-ARDS on the day of admission, day 3, and day 7. About 15 or 52 cytokines showed significant difference between SP and SP-ARDS patients with controls or 13 between SP-ARDS with SP alone and controls, including bone morphogenetic protein-15 (BMP-15), chemokine (C-X-C motif) ligand 16 （CXCL16），趋化因子（C-X-C基序）受体3（CXCR3），白介素-6（IL-6），蛋白质NOV同源物（Nov/CCN3），Glypican 3，胰岛素样生长因子样生长因子的结合蛋白4（IGFBP-4）（IGFBP-4）（IGFBP-4），IL-5，IL-5，IL-5 RAPT，IL-5 RALPIN，IL-5 RALPIN，IL-2-2-2-2-2-2-2-2-1 Orexin B与数字评估评分系统（DESS）分数显着相关。 ARDS过表达IL-6，CXCL16或IGFBP-4的患者的住院时间明显更长，并且继发感染的发生率更高。我们还发现，这些介质的较高水平与肺癌患者的存活率差有关，并参与肺泡上皮细胞上皮间质转变的过程。我们的初步研究表明，作为临床生物信息学的一部分，将蛋白质组学特征与临床信息学的整合对于验证和优化疾病特异性和疾病阶段的生物标志物很重要。
本文的在线版本（doi：10.1007/s10565-016-9322-4）包含补充材料，可供授权用户使用。
Acute respiratory distress syndrome (ARDS) is a heterogeneous syndrome that occurs as a result of various risk factors, including either direct or indirect lung injury, and systemic inflammation triggered also by severe pneumonia (SP). SP-ARDS-associated morbidity and mortality remains high also due to the lack of disease-specific biomarkers. The present study aimed at identifying disease-specific biomarkers in SP or SP-ARDS by integrating proteomic profiles of inflammatory mediators with clinical informatics. Plasma was sampled from the healthy as controls or patients with SP infected with bacteria or infection-associated SP-ARDS on the day of admission, day 3, and day 7. About 15 or 52 cytokines showed significant difference between SP and SP-ARDS patients with controls or 13 between SP-ARDS with SP alone and controls, including bone morphogenetic protein-15 (BMP-15), chemokine (C-X-C motif) ligand 16 (CXCL16), chemokine (C-X-C motif) receptor 3 (CXCR3), interleukin-6 (IL-6), protein NOV homolog (NOV/CCN3), glypican 3, insulin-like growth factor binding protein 4 (IGFBP-4), IL-5, IL-5 R alpha, IL-22 BP, leptin, MIP-1d, and orexin B with a significant correlation with Digital Evaluation Score System (DESS) scores. ARDS patients with overexpressed IL-6, CXCL16, or IGFBP-4 had significantly longer hospital stay and higher incidence of secondary infection. We also found higher levels of those mediators were associated with poor survival rates in patients with lung cancer and involved in the process of the epithelial mesenchymal transition of alveolar epithelial cells. Our preliminary study suggested that integration of proteomic profiles with clinical informatics as part of clinical bioinformatics is important to validate and optimize disease-specific and disease-staged biomarkers. The online version of this article (doi:10.1007/s10565-016-9322-4) contains supplementary material, which is available to authorized users.