Domenici L, Pieri L, Gallè M B, Romagnoli P, Adembri C
Department of Anatomy, Histology and Forensic Medicine, University of Florence, Florence, Italy.
Pathobiology. 2004;71(2):59-69. doi: 10.1159/000074418.
Intratracheal endotoxin in rats causes acute lung injury. Here we have addressed the cellular physiopathology of lung recovery from that injury.
The lungs of 5 untreated rats and rats treated with intratracheal endotoxin from 2, 3, 5, 8 (5 rats each) and 15 days (2 rats) were studied by light and electron microscopy and immunohistochemistry.
In the acute phase there was a reduction in the aerated spaces (p < 0.01); diffuse infiltration of granulocytes and macrophages; hyperplasia of type-II pneumocytes, and hypertrophy of interstitial cells. Aerated spaces improved during recovery. In the early recovery phase (3-8 days) the compartmentalization of infiltrating cells varied significantly (p < 0.01): macrophages remained widespread while neutrophils were inside blood vessels. Many pneumocytes were intermediate between type-I and type-II cells. In the late recovery phase (15 days) the infiltrate disappeared; myofibroblasts were significantly more than previously (p < 0.01) and extracellular matrix was abundant; type-II pneumocytes contained non-lamellated lipid inclusions.
Macrophages play a pivotal role in the damage-repair processes of the lung following endotoxin injury, leading to an increase in extracellular matrix, differentiation of myofibroblasts and altered secretion of surfactant by newly differentiated type-II pneumocytes.
大鼠气管内注入内毒素可导致急性肺损伤。在此，我们探讨了肺从该损伤中恢复的细胞生理病理学机制。
对5只未经处理的大鼠以及分别于注入气管内毒素后2天、3天、5天、8天（每组5只）和15天（2只）的大鼠的肺组织进行光镜、电镜及免疫组化研究。
急性期，肺充气空间减少（p < 0.01）；粒细胞和巨噬细胞弥漫性浸润；Ⅱ型肺细胞增生，间质细胞肥大。恢复过程中充气空间有所改善。在恢复早期（3 - 8天），浸润细胞的分布有显著差异（p < 0.01）：巨噬细胞仍广泛分布，而中性粒细胞位于血管内。许多肺细胞介于Ⅰ型和Ⅱ型细胞之间。在恢复后期（15天），浸润消失；肌成纤维细胞显著多于之前（p < 0.01），细胞外基质丰富；Ⅱ型肺细胞含有非层状脂质包涵体。
巨噬细胞在内毒素损伤后肺的损伤 - 修复过程中起关键作用，导致细胞外基质增加、肌成纤维细胞分化以及新分化的Ⅱ型肺细胞表面活性物质分泌改变。
