Department of Medical Virology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Immun Inflamm Dis. 2024 Jun;12(6):e1302. doi: 10.1002/iid3.1302.
Severe cases of COVID-19 often lead to the development of acute respiratory syndrome, a critical condition believed to be caused by the harmful effects of SARS-CoV-2 on type II alveolar cells. These cells play a crucial role in producing pulmonary surfactants, which are essential for proper lung function. Specifically focusing on surfactant proteins, including Surfactant protein A (SP-A), Surfactant protein B, Surfactant protein C, and Surfactant protein D (SP-D), changes in the levels of pulmonary surfactants may be a significant factor in the pathological changes seen in COVID-19 infection.
This study aims to gain insights into surfactants, particularly their impacts and changes during COVID-19 infection, through a comprehensive review of current literature. The study focuses on the function of surfactants as prognostic markers, diagnostic factors, and essential components in the management and treatment of COVID-19.
In general, pulmonary surfactants serve to reduce the surface tension at the gas-liquid interface, thereby significantly contributing to the regulation of respiratory mechanics. Additionally, these surfactants play a crucial role in the innate immune system within the pulmonary microenvironment. Within the spectrum of COVID-19 infections, a compelling association is observed, characterized by elevated levels of SP-D and SP-A across a range of manifestations from mild to severe pneumonia. The sudden decline in respiratory function observed in COVID-19 patients may be attributed to the decreased synthesis of surfactants by type II alveolar cells.
Collectin proteins such as SP-A and SP-D show promise as biomarkers, offering potential avenues for predicting and monitoring pulmonary alveolar injury in the context of COVID-19. This clarification enhances our understanding of the molecular complexities contributing to respiratory complications in severe COVID-19 cases, providing a foundation for targeted therapeutic approaches using surfactants and refined clinical management strategies.
严重的 COVID-19 病例常导致急性呼吸综合征的发生,这种危急状况被认为是由 SARS-CoV-2 对 II 型肺泡细胞的有害影响引起的。这些细胞在产生肺表面活性剂方面发挥着关键作用,肺表面活性剂对于正常的肺功能至关重要。具体而言,肺表面活性剂蛋白,包括表面活性物质蛋白 A(SP-A)、表面活性物质蛋白 B、表面活性物质蛋白 C 和表面活性物质蛋白 D(SP-D)的变化,可能是 COVID-19 感染中观察到的病理变化的一个重要因素。
通过对当前文献的综合回顾,本研究旨在深入了解表面活性剂,特别是它们在 COVID-19 感染中的作用和变化。本研究重点关注表面活性剂作为预后标志物、诊断因素以及在 COVID-19 管理和治疗中的重要组成部分的功能。
一般来说,肺表面活性剂的作用是降低气液界面的表面张力,从而对呼吸力学的调节起到重要作用。此外,这些表面活性剂在肺微环境中的固有免疫系统中发挥着关键作用。在 COVID-19 感染谱中,观察到一种强烈的关联,表现为从轻度到重度肺炎的各种表现中 SP-D 和 SP-A 水平升高。COVID-19 患者呼吸功能的突然下降可能归因于 II 型肺泡细胞合成表面活性剂的减少。
集落刺激因子蛋白如 SP-A 和 SP-D 作为生物标志物具有潜力,可以为预测和监测 COVID-19 中的肺肺泡损伤提供潜在途径。这一澄清增强了我们对导致严重 COVID-19 病例呼吸并发症的分子复杂性的理解,为使用表面活性剂和精细临床管理策略进行靶向治疗方法提供了基础。