Division of Pediatric Pulmonology, Chang Gung Memorial Hospital at Linkou, College of Medicine , Chang Gung University , Taoyuan 333 , Taiwan.
Department of Pediatrics, Chang Gung Memorial Hospital at Keelung, College of Medicine , Chang Gung University , Taoyuan 333 , Taiwan.
J Proteome Res. 2019 Mar 1;18(3):1248-1254. doi: 10.1021/acs.jproteome.8b00864. Epub 2019 Feb 19.
Fibrin formation in infectious parapneumonic effusion (IPE) characterizes complicated parapneumonic effusion and is important for providing guidelines for the management of IPEs that require aggressive interventions. We aim to identify metabolic mechanisms associated with bacterial invasion, inflammatory cytokines, and biochemical markers in cases of fibrinous infectious pleural effusions in children with pneumonia. Pleural fluid metabolites were determined by H nuclear magnetic resonance spectroscopy. Metabolites that contributed to the separation between fibrinous and nonfibrinous IPEs were identified using supervised partial least squares discriminant analysis ( Q/ R = 0.84; P < 0.01). IL-1β in the inflammatory cytokines and glucose in the biochemical markers were significantly correlated with 11 and 9 pleural fluid metabolites, respectively, and exhibited significant overlaps. Four metabolites, including glucose, lactic acid, 3-hydroxybutyric acid, and hypoxanthine, were significantly correlated with plasminogen activator inhibitor type 1 in the fibrinolytic system enzymes. Metabolic pathway analysis revealed that anaerobic bacterial fermentation with increased lactic acid and butyric acid via glucose consumption and adenosine triphosphate hydrolysis with increased hypoxanthine appeared to be associated with fibrinous IPE. Our results demonstrate that an increase in lactic acid anaerobic fermentation and hypoxanthine accumulation under hypoxic conditions are associated with fibrin formation in IPE, representing advanced pleural inflammatory progress in children with pneumonia.
纤维蛋白在感染性脓胸性胸腔积液（IPE）中的形成是复杂性脓胸的特征，对于为需要积极干预的 IPE 管理提供指导方针非常重要。我们旨在确定与肺炎患儿纤维蛋白性传染性胸腔积液中细菌入侵、炎症细胞因子和生化标志物相关的代谢机制。通过 H 核磁共振波谱法测定胸腔积液代谢物。使用有监督的偏最小二乘判别分析（ Q/ R = 0.84；P < 0.01）确定导致纤维蛋白性和非纤维蛋白性 IPE 分离的代谢物。炎症细胞因子中的白细胞介素 1β和生化标志物中的葡萄糖分别与 11 种和 9 种胸腔积液代谢物显著相关，并且表现出显著的重叠。四种代谢物，包括葡萄糖、乳酸、3-羟基丁酸和次黄嘌呤，与纤维蛋白溶解系统酶中的纤溶酶原激活物抑制剂 1 显著相关。代谢途径分析表明，葡萄糖消耗导致的无氧细菌发酵增加了乳酸和丁酸，三磷酸腺苷水解增加了次黄嘌呤，似乎与纤维蛋白性 IPE 有关。我们的结果表明，在缺氧条件下，乳酸无氧发酵和次黄嘌呤积累的增加与 IPE 中的纤维蛋白形成有关，代表肺炎患儿胸腔炎症的进展。
