Peng Bihao, Qiu Xiaojian, Dong Zhiwu, Zhang Jie, Pei Yinghua, Wang Ting
The Second Clinical Medical College, Nanchang University, Nanchang, Jiangxi 330000, P.R. China.
Department of Pulmonary Diseases, Beijing Tian Tan Hospital, Capital Medical University, Beijing 100050, P.R. China.
Exp Ther Med. 2021 Jan;21(1):63. doi: 10.3892/etm.2020.9495. Epub 2020 Nov 19.
Tracheobronchial tuberculosis (TB) leads to airway stenosis, irreversible airway damage and even death. The present study aimed to identify biomarkers for the diagnosis of tracheobronchial stenosis (TBS) secondary to tracheobronchial TB. A cohort was recruited, including patients with TBS after tracheobronchial TB, TBS after tracheal intubation or tracheotomy (TIT) and no stenosis of early-stage lung cancer,. Proteomic profiling was performed to gain insight into the mechanisms of the pathological processes. Differentially expressed proteins in the serum and bronchial alveolar lavage fluid (BALF) from patients were detected by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS). Subsequently, ELISA was performed to validate the changes of protein levels in an additional cohort. MALDI-TOF MS revealed that 8 peptides in the serum, including myeloid-associated differentiation marker, keratin type I cytoskeletal 18, fibrinogen α-chain, angiotensinogen (AGT), apolipoprotein A-I (APOAI), clusterin and two uncharacterized peptides, and nine peptides in BALF, including argininosuccinate lyase, APOAI, AGT and five uncharacterized peptides, were differentially expressed (molecular-weight range, 1,000-10,000 Da) in the TB group compared with the TIT group. The ELISA results indicated that the changes in the protein levels had a similar trend as those identified by proteomic profiling. In conclusion, the present study identified proteins that may serve as potential biomarkers and provide novel insight into the molecular mechanisms underlying TBS after tracheobronchial TB.
气管支气管结核可导致气道狭窄、不可逆的气道损伤甚至死亡。本研究旨在确定用于诊断气管支气管结核继发气管支气管狭窄（TBS）的生物标志物。招募了一个队列，包括气管支气管结核后发生TBS的患者、气管插管或气管切开术后发生TBS（TIT）的患者以及早期肺癌无狭窄的患者。进行蛋白质组分析以深入了解病理过程的机制。通过基质辅助激光解吸电离飞行时间质谱（MALDI-TOF MS）检测患者血清和支气管肺泡灌洗液（BALF）中差异表达的蛋白质。随后，进行酶联免疫吸附测定（ELISA）以验证另一队列中蛋白质水平的变化。MALDI-TOF MS显示，与TIT组相比，结核组血清中有8种肽差异表达（分子量范围为1000-10000 Da），包括髓系相关分化标志物、角蛋白I型细胞骨架18、纤维蛋白原α链、血管紧张素原（AGT）、载脂蛋白A-I（APOAI）、簇集素和两种未鉴定的肽；BALF中有9种肽差异表达，包括精氨琥珀酸裂解酶、APOAI、AGT和5种未鉴定的肽。ELISA结果表明，蛋白质水平的变化与蛋白质组分析确定的变化趋势相似。总之，本研究鉴定出了可能作为潜在生物标志物的蛋白质，并为气管支气管结核后TBS的分子机制提供了新的见解。
