Rhodes G C, Tapsall J W, Lykke A W
School of Pathology, University of New South Wales, Kensington, Australia.
J Pathol. 1989 Apr;157(4):347-57. doi: 10.1002/path.1711570412.
We describe an experimental model of pneumonia in Wistar rats evoked by Streptococcus sanguis. The lesion developed rapidly as a confluent bronchopneumonia of the single-lobed left lung. Except at the extreme base, where an abscess formed, the pneumonic process thereafter resolved, and most of the lung appeared microscopically and ultrastructurally normal 8 days after infection. Sequential electron microscopic studies revealed that in the areas of lung which subsequently resolved, damage was restricted to type 1 pneumocytes. Within 24 h of infection, the unaffected type 2 pneumocytes were observed to proliferate, transform into elongated pneumocytes of intermediate morphology, and then undermine and strip off the damaged type 1 cells from the subjacent basement membrane. Thereafter, the intermediate type pneumocytes completed their transformation into definitive type 1 cells, thus completing the repair process. We hypothesize that this represents an accelerated form of the normal type 1 replacement mechanism, and that uncomplicated epithelial repair following acute alveolar damage is possible if type 2 pneumocytes escape significant damage, so that they retain their capacity to proliferate and differentiate into type 1 epithelium.
我们描述了一种由血链球菌诱发的Wistar大鼠肺炎实验模型。病变迅速发展为左肺单叶融合性支气管肺炎。除了在形成脓肿的肺底部极端区域外，肺炎进程随后消退，感染8天后，大部分肺在显微镜和超微结构上看起来正常。连续电子显微镜研究显示，在随后消退的肺区域，损伤仅限于Ⅰ型肺泡上皮细胞。感染后24小时内，观察到未受影响的Ⅱ型肺泡上皮细胞增殖，转变为形态介于两者之间的细长型肺泡上皮细胞，然后从下方基底膜破坏并剥离受损的Ⅰ型细胞。此后，中间型肺泡上皮细胞完成向成熟Ⅰ型细胞的转变，从而完成修复过程。我们推测，这代表了正常Ⅰ型细胞替代机制的加速形式，并且如果Ⅱ型肺泡上皮细胞免受严重损伤，从而保留其增殖和分化为Ⅰ型上皮细胞的能力，那么急性肺泡损伤后简单的上皮修复是可能的。
