Lanken P N, Minda M, Pietra G G, Fishman A P
Am J Pathol. 1980 Jun;99(3):561-88.
In order to characterize the alveolar response to Pneumocystis carinii pneumonia, light and electron miscropy were used to trace the development of experimental infections with P carinii in rats treated with cortisone acetate and a low-protein diet. The first changes were found by the eighth day of treatment and consisted of the selective attachment of Pneumocystis organisms, mostly trophozoites, to alveolar Type 1 pneumocytes; the host cells were undamaged, and no inflammatory response was seen. After approximately one month of treatment, the seemingly innocuous host-parasite interaction was succeeded by focal necrosis of the Type 1 pneumocytes adjacent to organisms; hyperplasia of nearby Type 2 pneumocytes also occurred, to replace the dead Type 1 pneumocytes. Even at this stage, inflammatory reaction was conspicuously absent except for occasional alveolar macrophages in the diseased alveoli; in addition, all cells of the alveolar-capillary membrane other than Type 1 pneumocytes appeared entirely normal. Not only does the present study clarify the nature of alveolar injury caused by Pneumocystis carinii, but it also provides an experimental animal model in which selective injury of the alveolar lining cells occurs.
为了描述肺泡对卡氏肺孢子虫肺炎的反应,利用光镜和电镜追踪了用醋酸可的松和低蛋白饮食处理的大鼠实验性卡氏肺孢子虫感染的发展过程。在处理的第8天发现了最初的变化,包括卡氏肺孢子虫生物体(主要是滋养体)选择性地附着于Ⅰ型肺泡上皮细胞;宿主细胞未受损,未见炎症反应。处理约1个月后,这种看似无害的宿主-寄生虫相互作用被紧邻生物体的Ⅰ型肺泡上皮细胞局灶性坏死所取代;附近的Ⅱ型肺泡上皮细胞也发生增生,以取代死亡的Ⅰ型肺泡上皮细胞。即使在这个阶段,除了患病肺泡中偶尔出现的肺泡巨噬细胞外,明显没有炎症反应;此外,除Ⅰ型肺泡上皮细胞外,肺泡-毛细血管膜的所有细胞看起来完全正常。本研究不仅阐明了卡氏肺孢子虫引起的肺泡损伤的性质,还提供了一个肺泡衬里细胞发生选择性损伤的实验动物模型。