％0刊杂志，索非亚％A ODQvist，Lina％潜水员，莎拉％Ariise，Rebecca％A Abdillahi，Suado％A Wingren，Cecilia％的Lindmark，Helena％A Wellner，Annika％A leundin，索菲亚％yrlid，linda％a斧头，elisabeth％djukanovic，ratko％a sridhar，sriram％a higham，Andrew％a singh，Dave％a Southworth，Thomas％a brightling，Christopher E.％A Olsson，Henric K.％aJEVNIKAR，ZALA％T多OMICS链接IL-6逆向信号与中性粒细胞细胞外陷阱形成和嗜血杆子COPD％d 2021％R 10.1183 / 13993003.03312-2020％J.03312-2020％J欧洲呼吸轴颈％P2003312％X背景IL-6反式信号传导（IL-6Ts）作为慢性呼吸系统疾病的致病机制，但是司机IL-6TS在呼吸道中的IL-6TS和IL-6TS途径激活增加的患者的表型特征仍然很糟糕。目的我们的目的是识别和表征COPD患者，患者增加了IL-6，并阐明了IL-6TS途径的生物司机Activation.Methods我们使用了IL-6TS特异性痰生物标志物轮廓（SIL-6R，IL-6，IL-1β，IL-8，MIP-1β），将来自COPD患者的痰数据分层（n = 74; beat-COPD）通过分层群集。IL-6TS签名与临床特征和痰微生物谱有关。在人中性粒细胞中研究了中性粒细胞细胞外阱形成（Netosis）和IL-6Ts的诱导。结果分层聚类显示了COPD患者的IL-6TS高级子集（n = 24），其与IL共享表型特征-6ts-high子集以前在哮喘中识别。该子集的特征在于痰细胞计数增加（p = 0.0001），持续的痰性嗜菌菌（P = 0.0004），降低了寿命质量（CRQ总分; P = 0.008），并且痰液中的促炎介质和MMP水平增加。IL-6TS-HIGH COPD患者显示出植物产生的增加，嗜血杆菌作为主导属。甲型甲酰胺诱导的Netisis鉴定为增加可溶性IL-6受体（SIL-6R）水平的潜在机制。这是通过来自COPD患者的支气管肺泡灌洗液中SIL-6R与Netosiss标志物之间的显着正相关的支持。COPD患者的慢性殖民化引起的联系IL-6TS途径活化可能是COPD患者的一部分重要疾病司机.Footnotesthis手稿最近被接受在欧洲呼吸杂志中出版。 It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article.Conflict of interest: Dr. Winslow reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Odqvist reports personal fees Astrazeneca, outside the submitted work.Conflict of interest: Dr. Diver has nothing to disclose.Conflict of interest: Dr. Riise reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Abdillahi reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Wingren reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Lindmark reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Wellner reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Lundin reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Yrlid reports other from AstraZeneca, outside the submitted work.Conflict of interest: Ms. Ax is an employee of, and hold stock/stock options, in AstraZeneca, which supported the study.Conflict of interest: Dr. Djukanovic reports personal fees from TEVA, personal fees from TEVA, personal fees from Novartis, personal fees from Novartis, personal fees from Synairgen, personal fees from GlaxoSmithKline, outside the submitted work.Conflict of interest: Dr. Sridhar reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Higham has nothing to disclose.Conflict of interest: Dr. Singh reports personal fees from AstraZeneca, personal fees from Boehringer Ingelheim, personal fees from Chiesi, personal fees from Cipla, personal fees from Genentech, personal fees from GlaxoSmithKline, personal fees from Glenmark, personal fees from Gossamerbio, personal fees from Menarini, personal fees from Mundipharma, personal fees from Novartis, personal fees from Peptinnovate, personal fees from Pfizer, personal fees from Pulmatrix, personal fees from Theravance, personal fees from Verona, outside the submitted work.Conflict of interest: Dr. Southworth has nothing to disclose.Conflict of interest: Dr. Brightling reports personal fees from GSK, personal fees from AzstraZeneca/MedImmune, personal fees from Boehringer Ingelheim, personal fees from Novartis, personal fees from Roche, personal fees from Chiesi, outside the submitted work.Conflict of interest: Dr. Olsson reports other from AstraZeneca, outside the submitted work.Conflict of interest: Dr. Jevnikar Rojnik reports and employee of, and hold stock/stock options, in AstraZeneca, which supported the study. %U //www.qdcxjkg.com/content/erj/early/2021/03/10/13993003.03312-2020.full.pdf