钙结合蛋白S100A12与中性粒细胞胞外诱捕网形成在重症肺结核患者肺损伤中作用机制研究进展  

Research progresses on the role and mechanism of calcium-binding protein S100A12 and neutrophil extracellular trap formation in lung injury of severe pulmonary tuberculosis patients

作　　者：宋云林[1] 布祖克拉·阿布都艾尼 王桂荣[2] 张继园 鲁晓擘[4] Song Yunlin;Buzukela Abuduaini;Wang Guirong;Zhang Jiyuan;Lu Xiaobo(Department of Intensive Care Unit,the First Affiliated Hospital of Xinjiang Medical University,Urumqi 830013,China;Department of Laboratory Medicine,Beijing Chest Hospital,Capital Medical University,Beijing 101149,China;First Clinical Institute of Xinjiang Medical University,Urumqi 830013,China;Center of Infection,the First Affiliated Hospital of Xinjiang Medical University,Urumqi 830013,China)

机构地区：[1]新疆医科大学第一附属医院重症医学中心,乌鲁木齐830013 [2]首都医科大学附属北京胸科医院检验科,北京101149 [3]新疆医科大学第一临床医学院,乌鲁木齐830013 [4]新疆医科大学第一附属医院感染中心,乌鲁木齐830013

出　　处：《中国防痨杂志》2025年第4期513-519,共7页Chinese Journal of Antituberculosis

基　　金：国家自然科学基金(82360381);省部共建中亚高发病成因与防治国家重点实验室开放课题(SKL-HIDCA-2021-JH13)。

摘　　要：重症肺结核患者的发病率和死亡率居高不下,然而,由于重症肺结核在早期阶段的临床症状和体征缺乏特异性,诊断面临巨大挑战。此外,重症肺结核的治疗也因药物相互作用、药物与疾病相互作用及药物不良反应等多重因素的影响变得更加复杂,这些因素对结核病的预防和控制带来了新的挑战。重症肺结核的发病机制涉及到宿主与结核分枝杆菌间复杂的交互作用,发病机制仍不完全清楚。有研究报道,钙结合蛋白S100A12(简称“S100A12”)与中性粒细胞胞外诱捕网(neutrophil extracellular traps,NETs)在重症肺结核的病理生理过程中扮演着至关重要的角色,S100A12驱动NETs形成,是NETs生理病理效应相关的关键蛋白。S100A12通过调控免疫细胞与炎症因子的释放及其相互作用,参与重症肺结核患者肺功能损伤机制,然而,当前针对S100A12与NETs在重症肺结核调控中的机制尚未完全阐明。鉴于此,笔者旨在综述S100A12与NETs在重症肺结核患者中的相关研究进展及其潜在的分子机制,以期为重症肺结核治疗策略的探索提供新的科学依据和创新性思路。The incidence and mortality rates of severe pulmonary tuberculosis remain persistently high.However,the disease face significant diagnostic challenges due to the lack of specificity in clinical signs and symptoms during the early stages of the disease.Furthermore,the therapeutic of severe tuberculosis has become being complicated due to multiple factors,such as drug-drug interactions,drug-disease interactions,and adverse drug reactions,all of which together pose new challenges for tuberculosis prevention and control.The pathogenesis of severe tuberculosis involves a complex interaction between the host and Mycobacterium tuberculosis,yet the mechanism of pathogenesis remains incompletely understood.Recent studies indicate that calcium-binding protein S100A12(hereafter“S100A12”)and neutrophil extracellular traps(NETs)are essential in developing severe tuberculosis.S100A12 drives the formation of NETs,and serve as a key protein mediating the physiopathological effects of NETs.S100A12 contributes to the mechanism of lung function injury in severe tuberculosis patients through regulation the release of immune cells,inflammatory cytokine release,and their interaction.Nevertheless,the regulatory mechanisms of S100A12 and NETs in severe tuberculosis pathogenesis has not been fully elucidated.Given this,this review aims to comprehensively summarize the research progress on S100A12 and NETs in severe tuberculosis and their potential molecular mechanisms to provide a new scientific basis and innovative insights for exploring therapeutic strategies for severe tuberculosis.

关 键 词：中性粒细胞 结核 肺 肺损伤 作用机制 

分 类 号：R521[医药卫生—内科学]