Adamson I Y, Bowden D H
Am J Pathol. 1977 Jun;87(3):569-80.
Bleomycin is known to induce diffuse pulmonary fibrosis and epithelial metaplasia. The reaction of the alveolar epithelium following a single intravenous or multiple intraperitoneal injections of bleomycin to mice is now examined in a combined morphologic and cytodynamic study. Necrosis of Type 1 cells was observed, followed by proliferation of Type 2 cells, a common reparative process. The proliferated cells transformed to a variety of epithelial forms, including ciliated cells and cells with morphologic features intermediate between alveolar and bronchiolar epithelium. No evidence of cell injury or increased cell division was found in the bronchial epithelium. It is concluded that the metaplastic ciliated epithelial cells are produced by an abnormal reparative process in the alveolar epithelium. The results suggest that, whereas the "resting" Type 2 cell is not vulnerable to bleomycin, in the postmitotic phase the drug may modify the synthetic mechanisms of cellular differentiation and thereby induce metaplasia.
博来霉素已知可诱发弥漫性肺纤维化和上皮化生。现通过形态学和细胞动力学联合研究，检测单次静脉注射或多次腹腔注射博来霉素后小鼠肺泡上皮的反应。观察到Ⅰ型细胞坏死，随后Ⅱ型细胞增殖，这是一种常见的修复过程。增殖的细胞转变为多种上皮形式，包括纤毛细胞以及形态特征介于肺泡上皮和细支气管上皮之间的细胞。在支气管上皮中未发现细胞损伤或细胞分裂增加的证据。得出的结论是，化生的纤毛上皮细胞是由肺泡上皮异常修复过程产生的。结果表明，虽然“静止”的Ⅱ型细胞对博来霉素不敏感，但在有丝分裂后期，该药物可能会改变细胞分化的合成机制，从而诱导化生。
