Department of Medicine, SUNY Downstate Health Sciences University, Brooklyn, NY, 11203, USA.
Lipids Health Dis. 2020 Jun 3;19(1):122. doi: 10.1186/s12944-020-01278-8.
Lung lipid metabolism participates both in infant and adult pulmonary disease. The lung is composed by multiple cell types with specialized functions and coordinately acting to meet specific physiologic requirements. The alveoli are the niche of the most active lipid metabolic cell in the lung, the type 2 cell (T2C). T2C synthesize surfactant lipids that are an absolute requirement for respiration, including dipalmitoylphosphatidylcholine. After its synthesis and secretion into the alveoli, surfactant is recycled by the T2C or degraded by the alveolar macrophages (AM). Surfactant biosynthesis and recycling is tightly regulated, and dysregulation of this pathway occurs in many pulmonary disease processes. Alveolar lipids can participate in the development of pulmonary disease from their extracellular location in the lumen of the alveoli, and from their intracellular location in T2C or AM. External insults like smoke and pollution can disturb surfactant homeostasis and result in either surfactant insufficiency or accumulation. But disruption of surfactant homeostasis is also observed in many chronic adult diseases, including chronic obstructive pulmonary disease (COPD), and others. Sustained damage to the T2C is one of the postulated causes of idiopathic pulmonary fibrosis (IPF), and surfactant homeostasis is disrupted during fibrotic conditions. Similarly, surfactant homeostasis is impacted during acute respiratory distress syndrome (ARDS) and infections. Bioactive lipids like eicosanoids and sphingolipids also participate in chronic lung disease and in respiratory infections. We review the most recent knowledge on alveolar lipids and their essential metabolic and signaling functions during homeostasis and during some of the most commonly observed pulmonary diseases.
肺脂质代谢参与婴儿和成人肺部疾病。肺由具有特定功能的多种细胞类型组成，它们协调作用以满足特定的生理需求。肺泡是肺中最活跃的脂质代谢细胞——Ⅱ型细胞（T2C）的栖息地。T2C 合成肺表面活性物质脂质，这是呼吸的绝对要求，包括二棕榈酰磷脂酰胆碱。在合成并分泌到肺泡后，T2C 或肺泡巨噬细胞（AM）可回收表面活性剂。表面活性剂的生物合成和回收受到严格调控，该途径的失调发生在许多肺部疾病过程中。肺泡脂质可以从其在肺泡腔中的细胞外位置以及从 T2C 或 AM 的细胞内位置参与肺部疾病的发生。外部刺激物，如烟雾和污染，会干扰表面活性剂的动态平衡，导致表面活性剂不足或积累。但是，在许多慢性成人疾病中，包括慢性阻塞性肺疾病（COPD）等，也观察到表面活性剂动态平衡的破坏。T2C 的持续损伤是特发性肺纤维化（IPF）的一个假设原因，在纤维化条件下，表面活性剂的动态平衡被破坏。同样，在急性呼吸窘迫综合征（ARDS）和感染期间，表面活性剂的动态平衡也受到影响。类二十烷酸和鞘脂等生物活性脂质也参与慢性肺部疾病和呼吸道感染。我们综述了肺泡脂质及其在稳态和一些最常见观察到的肺部疾病中的基本代谢和信号功能的最新知识。
