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实验性军团病中肺泡和巨噬细胞的超微结构

Ultrastructure of pulmonary alveoli and macrophages in experimental Legionnaires' disease.

作者信息

Baskerville A, Dowsett A B, Fitzgeorge R B, Hambleton P, Broster M

出版信息

J Pathol. 1983 Jun;140(2):77-90. doi: 10.1002/path.1711400202.

DOI:10.1002/path.1711400202
PMID:6854436
Abstract

Guinea pigs, rhesus monkeys and marmosets infected with Legionella pneumophila in small particle aerosols developed an acute fibrinopurulent bronchopneumonia. Changes from 24 hr included exudation into alveoli of protein-rich, often fibrinous fluid and many polymorphonuclear leucocytes (PMN) and macrophages. Damage to alveolar capillary endothelium consisted of widespread cytoplasmic swelling and vesiculation, but necrosis of endothelium and the associated alveolar epithelium was focal and less common. Phagocytosis of L. pneumophila organisms was predominantly by macrophages, but the bacteria were also seen in PMN. Free organisms were present in alveoli and capillary lumina at all stages of the infection but were not observed in lung parenchymal cells. Some infected macrophages and PMN became necrotic and lysed to release intact bacteria. In all species of experimental animal, intracytoplasmic aggregations of granular material, believed to be glycogen, were seen frequently in macrophages and PMN which had phagocytosed L. pneumophila. These deposits of glycogen may reflect either an increased energy demand by the host cell or an interference with its carbohydrate metabolism.

摘要

豚鼠、恒河猴和狨猴吸入含有嗜肺军团菌的小颗粒气溶胶后,会患上急性纤维蛋白脓性支气管肺炎。感染24小时后的变化包括富含蛋白质(常为纤维蛋白性)的液体以及许多多形核白细胞(PMN)和巨噬细胞渗出到肺泡中。肺泡毛细血管内皮细胞的损伤表现为广泛的细胞质肿胀和空泡化,但内皮细胞及相关肺泡上皮细胞的坏死是局灶性的,且较少见。嗜肺军团菌主要被巨噬细胞吞噬,但在PMN中也可见到细菌。在感染的各个阶段,肺泡和毛细血管腔内均存在游离的细菌,但在肺实质细胞中未观察到。一些被感染的巨噬细胞和PMN发生坏死并溶解,释放出完整的细菌。在所有实验动物物种中,在吞噬了嗜肺军团菌的巨噬细胞和PMN中,经常可见到被认为是糖原的颗粒状物质的胞质内聚集。这些糖原沉积物可能反映了宿主细胞能量需求的增加或其碳水化合物代谢受到干扰。

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