代谢组学
蛋白质组学
代谢组
肺结核
串联质量标签
生物
定量蛋白质组学
结核分枝杆菌
重编程
肺结核
计算生物学
生物信息学
代谢途径
转录组
组学
折叠变化
脂质代谢
医学
免疫学
新陈代谢
临床意义
串联质谱法
病理
蛋白质-蛋白质相互作用
生物标志物
细胞生物学
生物途径
通路分析
肺部感染
作者
Jianhai Wang,Dong Zhang,Chong Du,Haibai Sun,Chunfeng Liu,Yuming Li,Zhoumao Cairang,Ru Li,Gazang Zhuoma,Jun Ma,Qingcuo Ren,Xin Sun,Huaiyong Chen
标识
DOI:10.1021/acs.jproteome.5c00656
摘要
infection and is associated with poor treatment response and high transmissibility. To capture the systemic disturbances that accompany cavity formation, we profiled sera from 30 cPTB patients, 30 noncavitary PTB patients, and 30 matched healthy volunteers using proximity-extension proteomics and untargeted ultraperformance liquid-chromatography tandem mass spectrometry. Multigroup analysis revealed broad suppression of cell-junction proteins and rewiring of amino-acid and lipid metabolism in PTB; these changes were accentuated in cPTB, where 15 cardiomyocyte-associated proteins and fifty-nine metabolites differed significantly from noncavitary PTB. Integrated network mapping converged on two consistently down-regulated molecules─desmoglein-4 (DSG4) and amyl salicylate─whose combined abundance showed moderate discrimination of cPTB from noncavitary PTB (AUC = 0.738). These findings are consistent with cavity formation being associated with perturbations in cardiovascular-related pathways and broad metabolic reprogramming, and they nominate the DSG4-amyl salicylate pair as an exploratory, hypothesis-generating signature that requires validation in independent cohorts before any clinical interpretation or host-directed therapeutic use.
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