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Alveolar-Capillary Membrane-Related Pulmonary Cells as a Target in Endotoxin-Induced Acute Lung Injury

机译:肺泡-毛细血管膜相关的肺细胞作为内毒素诱导的急性肺损伤的靶标。

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摘要

The main function of the lungs is oxygen transport from the atmosphere into the blood circulation, while it is necessary to keep the pulmonary tissue relatively free of pathogens. This is a difficult task because the respiratory system is constantly exposed to harmful substances entering the lungs by inhalation or via the blood stream. Individual types of lung cells are equipped with the mechanisms that maintain pulmonary homeostasis. Because of the clinical significance of acute respiratory distress syndrome (ARDS) the article refers to the physiological role of alveolar epithelial cells type I and II, endothelial cells, alveolar macrophages, and fibroblasts. However, all these cells can be damaged by lipopolysaccharide (LPS) which can reach the airspaces as the major component of the outer membrane of Gram-negative bacteria, and lead to local and systemic inflammation and toxicity. We also highlight a negative effect of LPS on lung cells related to alveolar-capillary barrier and their response to LPS exposure. Additionally, we describe the molecular mechanism of LPS signal transduction pathway in lung cells.
机译:肺的主要功能是氧气从大气中进入血液循环,同时有必要保持肺组织相对不含病原体。这是一项艰巨的任务,因为呼吸系统始终会通过吸入或通过血流接触进入肺部的有害物质。个别类型的肺细胞配备了维持肺稳态的机制。由于急性呼吸窘迫综合征(ARDS)的临床意义,本文指的是I型和II型肺泡上皮细胞,内皮细胞,肺泡巨噬细胞和成纤维细胞的生理作用。但是,所有这些细胞都可能受到脂多糖(LPS)的破坏,脂多糖可作为革兰氏阴性细菌外膜的主要成分到达空气空间,并导致局部和全身性炎症和毒性。我们还强调了LPS对与肺泡-毛细血管屏障相关的肺细胞及其对LPS暴露的反应的负面影响。此外,我们描述了肺细胞中LPS信号转导途径的分子机制。

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