Atwal O S, Minhas K J, Perry M S
Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Canada.
Histol Histopathol. 1988 Jul;3(3):301-14.
The alveolar type I cell is a major permeability barrier between the pulmonary interstitium and alveolar spaces and its thin cytoplasmic processes are greatly susceptible to injury. These cells are often observed to undergo progressive vesiculation, vacuolization and desquamation during 3-methylindole (3MI)-induced acute pulmonary edema after oral administration in goats and cattle. The present study describes proliferation of SER and the presence of polymerized tubulin in the form of microtubules arranged in large bundles shown at ultrastructural level as well as with immunofluorescence staining for tubulin in alveolar type I cells 72 hours after 3MI treatment. Such changes were not seen in pulmonary endothelial cells, alveolar type II cells, alveolar macrophages and neutrophils. The possible role of microtubules in alveolar type I cells as a mechanistic support to resist disruption against the forces of interstitial and alveolar edema is compared with alveolar type II cells, alveolar macrophages and neutrophils. The latter cells undergo dynamic movements in response to inflammatory stimuli and therefore did not show microtubules in their cytoplasm.
肺泡I型细胞是肺间质与肺泡腔之间的主要渗透屏障，其薄的细胞质突起极易受到损伤。在山羊和牛口服3-甲基吲哚（3MI）诱导的急性肺水肿过程中，常观察到这些细胞发生渐进性囊泡化、空泡化和脱屑。本研究描述了在3MI处理72小时后，肺泡I型细胞超微结构水平以及微管蛋白免疫荧光染色显示的滑面内质网增殖和以大束排列的微管形式存在的聚合微管蛋白。在肺内皮细胞、肺泡II型细胞、肺泡巨噬细胞和中性粒细胞中未观察到此类变化。将肺泡I型细胞中微管作为抵抗间质和肺泡水肿力量破坏的机械支撑的可能作用与肺泡II型细胞、肺泡巨噬细胞和中性粒细胞进行了比较。后几种细胞会对炎症刺激做出动态反应，因此其细胞质中未显示微管。
