ty -jour t1 -splunc1：囊性纤维化的新颖标记加剧JF-欧洲呼吸杂志JO -EUR RESSIR J DO -10.1183/13993003.00503.00507-2020 SP -2000507 AU -KHANAL -KHANAL -KHANAL，SARA，SARA AU -WEBSTER，MEGAN AU -NIU，NAIQIAN AUU -NAIQIAN AUU -NAIQIAN AUU -NAIQIAN AUU -NAIQIAN AUU -NAIQIAN AUU-Zielonka，Jana au -Nunez，Myra Au -Chupp，Geoffrey Au -Slade，Martin D. Au -Cohn，Lauren Au -Sauler，Maor Au -Gomez -Gomez，Jose L. Au -Au -Tarran，Robert Au -Sharma，Lokesh au -Sharma，Lokesh au -au -au -au -au -au-Dela Cruz，Charles S. Au -Egan，Marie au -Laguna，Theresa au -Britto，Clemente J. Y1-2021/01/01 Ur -http：//www.qdcxjkg.com/content/content/early/early/2021/04/01/13993003.00507-2020.Abstract N2-急性肺部恶化（AE）是囊性纤维化（CF）的临床恶化（CF）的发作，通常是由于感染而导致的。及时检测对于最大程度地减少发病率和与AE期间急性炎症相关的肺功能下降至关重要。基于我们以前的观察，气道蛋白短pa肺鼻音上皮克隆1（SPLUNC1）受炎症信号的调节，我们调查了使用Splunc1波动来诊断和预测CF中的AE的使用。我们从两个独立的同伴中招募了CF参与者，以测量AE AE AE。痰液中炎症和记录的临床结局的标志性标记为1年的随访期。SPLUNC1水平较高（n = 9，10.7μgml – 1），在没有AE的CF参与者中显着降低（n = 30）（n = 30），5.7μgml– 1，p = 0.016）。在AE期间，SPLUNC1的水平降低了71.9％（n = 14，1.6μgml – 1，p = 0.0034），无论年龄，性别，CF引起的突变或微生物学发现如何。AE中的细胞因子IL-1β和TNFα也增加了，而肺功能并未持续降低。稳定的CF参与者具有较低的SPLUNC1水平的参与者在60天后具有AE的可能性更大（HR：11.49，标准错误：0.83，p = 0.0033）。 Low-SPLUNC1 stable participants remained at higher AE risk even one year after sputum collection (HR: 3.21, Standard Error: 0.47, p=0.0125). SPLUNC1 was downregulated by inflammatory cytokines and proteases increased in sputum during AE.In acute CF care, low SPLUNC1 levels could support a decision to increase airway clearance or to initiate pharmacological interventions. In asymptomatic, stable patients, low SPLUNC1 levels could inform changes in clinical management to improve long-term disease control and clinical outcomes in CF.FootnotesThis manuscript has recently been accepted for publication in the European Respiratory Journal. 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. Khanal has nothing to disclose.Conflict of interest: Dr. Webster has nothing to disclose.Conflict of interest: Dr. Niu has nothing to disclose.Conflict of interest: Dr. Zielonka has nothing to disclose.Conflict of interest: MNunez has nothing to disclose.Conflict of interest: Dr. Chupp reports other from Genentech, other from Astra Zeneca, other from Sanofi - Regeneron, other from GSK, other from TEVA, other from Boehringer-Ingelheim, other from Circassia, outside the submitted work; .Conflict of interest: Dr. Slade has nothing to disclose.Conflict of interest: Dr. Cohn reports other from Genentech, other from Novartis, other from Astra-zeneca, other from GlaxoSmithKline, other from Regeneron, other from Pieris, other from Sanofi, outside the submitted work; .Conflict of interest: Dr. Sauler has nothing to disclose.Conflict of interest: Dr. Gomez has nothing to disclose.Conflict of interest: Dr. Tarran reports other from Eldec Pharmaceuticals, outside the submitted work; In addition, Dr. Tarran has a patent Peptide inhibitors of Ca2+ channels pending, a patent PEPTIDE INHIBITORS OF SODIUM CHANNELS with royalties paid, and a patent Regulation of sodium channels by PLUNC proteins with royalties paid.Conflict of interest: Dr. Sharma has nothing to disclose.Conflict of interest: Dr. Dela Cruz has nothing to disclose.Conflict of interest: Dr. Egan has nothing to disclose.Conflict of interest: Dr. Laguna reports grants from National Institutes of Health, grants from Cystic Fibrosis Foundation, other from Vertex Physician Advisory Board, outside the submitted work; .Conflict of interest: Dr. Britto has nothing to disclose. ER -