University of Michigan Medical School, Department of Pathology, Ann Arbor, Michigan, USA.
Ann N Y Acad Sci. 2010 Aug;1203:53-9. doi: 10.1111/j.1749-6632.2010.05552.x.
Oxidative stress in lung often occurs in humans during acute lung injury (ALI) and in the acute respiratory distress syndrome. The lung inflammatory response may proceed to the development of pulmonary fibrosis, a devastating complication that occurs in premature infants after prolonged exposure to high oxygen concentrations. Oxidant-related ALI can be induced by airway deposition of lipopolysaccharide or IgG immune complexes, resulting in activation of recruited neutrophils and residential macrophages, whose oxidants and proteases produce reversible ALI. In the presence of a powerful trigger of leukocytes (phorbol myristate acetate), or following intrapulmonary deposition of enzymes that generate oxidants, extensive endothelial and epithelial damage and destruction occurs, overwhelming repair mechanisms of lung and resulting in pulmonary fibrosis. How residential or circulating stem cells participate in regeneration of damaged/destroyed cells may provide clues regarding therapy in humans who are experiencing lung inflammatory damage.
肺中的氧化应激在人类急性肺损伤 (ALI) 和急性呼吸窘迫综合征中经常发生。肺炎症反应可能会发展为肺纤维化，这是一种破坏性的并发症，在早产儿长时间暴露于高浓度氧气后会发生。与氧化剂相关的 ALI 可通过气道沉积脂多糖或 IgG 免疫复合物引起，导致募集的中性粒细胞和驻留巨噬细胞被激活，其氧化剂和蛋白酶产生可逆性 ALI。在存在白细胞强触发物（十四烷酰佛波醇乙酸酯）的情况下，或在肺内沉积生成氧化剂的酶后，会发生广泛的内皮和上皮损伤和破坏，超过肺的修复机制，导致肺纤维化。驻留或循环干细胞如何参与受损/破坏细胞的再生，可能为正在经历肺炎症损伤的人类提供治疗线索。
