Rhodes G C, Lykke A W, Tapsall J W, Smith L W
School of Pathology, University of New South Wales, Kensington, Australia.
J Pathol. 1989 Nov;159(3):245-53. doi: 10.1002/path.1711590312.
We describe an experimental model in Wistar rats of non-resolving bronchopneumonia evoked by Streptococcus pneumoniae type 25. In contrast to a model of resolving streptococcal pneumonia that we have previously described, morphological studies reveal that in this model, there is significant early damage to type 1 pneumocytes which progresses to necrosis, leaving isolated areas of denuded alveolar basement membrane. Furthermore, there is accompanying degeneration and necrosis of a proportion of the type 2 pneumocytes, and alveolar epithelial repair by proliferation and differentiation of these cells appears to be retarded. Isolated, hypertrophic, and hyperplastic foci of type 2 pneumocytes persist as the acute inflammatory response subsides, and organization progresses with proliferation and emigration of fibroblasts into the lumina of alveoli and terminal bronchioles. The resultant lesion is morphologically indistinguishable from bronchiolitis obliterans organizing pneumonia. We hypothesize that the abnormal outcome in this model of pneumonia is a consequence of the failure of proliferating type 2 pneumocytes to transform into type 1 pneumocytes and thus maintain the integrity of the alveolar epithelial surface.
我们描述了一种由25型肺炎链球菌诱发的、在Wistar大鼠中建立的非消散性支气管肺炎实验模型。与我们之前描述的消散性链球菌肺炎模型不同，形态学研究显示，在该模型中，I型肺细胞早期即受到显著损伤，并进展为坏死，导致肺泡基底膜出现孤立的裸露区域。此外，一部分II型肺细胞出现变性和坏死，这些细胞通过增殖和分化进行的肺泡上皮修复似乎受到了阻碍。随着急性炎症反应消退，孤立的、肥大的和增生的II型肺细胞灶持续存在，随着成纤维细胞增殖并迁移至肺泡和终末细支气管腔，机化过程不断进展。最终形成的病变在形态上与机化性细支气管炎并机化性肺炎无法区分。我们推测，该肺炎模型中出现异常结果是由于增殖的II型肺细胞无法转化为I型肺细胞，从而无法维持肺泡上皮表面的完整性。
