Wilson N J, Gosney J R, Mayall F
Department of Pathology, University of Liverpool.
Thorax. 1993 Dec;48(12):1252-6. doi: 10.1136/thx.48.12.1252.
There is evidence to suggest, particularly from studies in animals, that the products of pulmonary endocrine cells, especially gastrin releasing peptide, may have a role in the pathogenesis of fibrosis in the lung. This study was carried out to examine the morphology, number, distribution, and content of pulmonary endocrine cells in tissue from 49 patients with diffuse pulmonary fibrosis.
Twenty patients with interstitial pneumonitis, 17 with early fibrosis, and 12 with frank honeycombing were studied, together with five age matched controls without pulmonary disease. Endocrine cells were immunolabeled by the avidin-biotin complex method for two general markers (protein gene product 9.5 and neuron specific enolase) and a range of normal and aberrant secretory products.
In the early stages, characterised by vigorous pneumonitis, endocrine cells were normal in appearance and distribution but very few in number. They contained only those secretory products normally found in such cells in health; inappropriate substances were not seen. By the time of early fibrosis endocrine cells were even fewer. None were identifiable in the lungs affected by honeycombing, despite the fact that all contained intact, well preserved epithelium.
It seems unlikely that the products of pulmonary endocrine cells can have any role in the pathogenesis of diffuse pulmonary fibrosis in man, the diminution in their number with advancing fibrosis probably reflecting their loss simply as a consequence of generalised epithelial damage.
有证据表明,尤其是来自动物研究的证据,肺部内分泌细胞的产物,特别是胃泌素释放肽,可能在肺部纤维化的发病机制中起作用。本研究旨在检查49例弥漫性肺纤维化患者组织中肺内分泌细胞的形态、数量、分布和含量。
研究了20例间质性肺炎患者、17例早期纤维化患者和12例明显蜂窝状改变患者,以及5名年龄匹配的无肺部疾病对照者。采用抗生物素蛋白-生物素复合物法对内分泌细胞进行免疫标记,检测两种通用标志物(蛋白质基因产物9.5和神经元特异性烯醇化酶)以及一系列正常和异常分泌产物。
在以剧烈肺炎为特征的早期阶段,内分泌细胞的外观和分布正常,但数量很少。它们仅含有健康状态下此类细胞中正常存在的分泌产物;未发现不适当的物质。到早期纤维化阶段,内分泌细胞更少。在出现蜂窝状改变的肺部,尽管所有肺组织都含有完整、保存良好的上皮,但均未发现可识别的内分泌细胞。
肺部内分泌细胞的产物似乎不太可能在人类弥漫性肺纤维化的发病机制中起任何作用,随着纤维化进展其数量减少可能仅仅反映了由于广泛的上皮损伤导致的细胞丢失。