论上呼吸道产生的病原微滴吸入性支气管传播的力学机制及其对感染发病的启示
On the mechanics of inhaled bronchial transmission of pathogenic microdroplets generated from the upper respiratory tract, with implications for infection onset
AI总结：
本研究通过基于CT的3D气道重建与LES气流模拟，探讨了上呼吸道黏膜液微滴在吸入后向深部肺部传输的力学机制，发现大于5微米的微滴仍能显著渗透至下呼吸道，揭示了其加速肺部感染定植的机制。
摘要：
上呼吸道（URT）黏膜液因黏弹性拉伸和断裂形成的微滴，在吸入下风处时，能否解释 URT 初始感染发生后深部肺部感染迅速出现的现象？尽管众所周知，从外部吸入的颗粒物只有直径 < 5 微米时才可能渗透到下呼吸道，但在吸入过程中从 URT 内部黏膜剪切脱落的颗粒物（许多直径 > 5 微米）的命运仍是一个悬而未决的问题。这些颗粒物主要起源于鼻咽部、口咽部以及带有声带的喉室。为解决所提出的问题，本研究采用基于 CT 的 3D 气道解剖重建，从喉部声带区域分离出该通道，映射整个气管腔，并在气管支气管树的第 2 级处终止。通过描绘的几何结构，使用 LES 方案进行气流模拟，以复制 15 L/min 的放松呼吸状态。针对环境空气通量，进行了数值实验，以监测直径为 1-30 微米的液体颗粒的传输，这些颗粒具有类似于含有病毒气溶胶化黏液的物理特性。传输到下呼吸道的全尺寸数值传输趋势被发现与降阶数学模型的结果一致，该模型通过在解剖引导的 2D 势流域中进行点涡理想化，概念化了气道内涡旋不稳定性对局部颗粒传输的影响。结果共同表明，即使 URT 衍生的颗粒物大至 10 和 15 微米，其深部肺部渗透趋势也显著升高。此类微滴携带到支气管空间的高病毒载量，可以从力学机制上解释肺部感染加速定植的现象。
英文摘要：
Could the microdroplets formed by viscoelastic stretching and break-up of mucosal liquids in the upper respiratory tract (URT), when inhaled further downwind, explain the brisk pace at which deep lung infections emerge following onset of initial infection at the URT? While it is well-established that particulates inhaled from outside can possibly penetrate to the lower airway only if they are < 5 microns, the fate of particulates (many > 5-microns in diameter) sheared away from the intra-URT mucosa during inhalation remains an open question. These particulates predominantly originate at the nasopharynx, oropharynx, and laryngeal chamber with the vocal folds. To resolve the posed question, this study considers a CT-based 3D anatomical airway reconstruction and isolates the tract from the laryngeal vocal fold region, mapping the entire tracheal cavity and concluding at generation 2 of the tracheobronchial tree. Through the delineated geometry, airflow simulation is conducted using the LES scheme to replicate relaxed inhalation at 15 L/min. Against the ambient air flux, numerical experiments have been performed to monitor the transport of liquid particulates with diameters 1-30 microns, bearing physical properties akin to aerosolized mucus with embedded virions. The full-scale numerical transmission trends to the lower airway were found consistent with the findings from a reduced-order mathematical model that conceptualized the impact of intra-airway vortex instabilities on local particle transport through point vortex idealization in an anatomy-guided 2D potential flow domain. The results collectively demonstrate markedly elevated trends of deep lung penetration by the URT-derived particulates, even if they are as large as 10- and 15 microns. The high viral load carried by such droplets to the bronchial spaces could mechanistically explain the accelerated seeding of infection in the lungs.
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