Castleman W L
Am J Pathol. 1984 Feb;114(2):322-35.
The ultrastructural and morphometric effects of viral respiratory disease during postnatal lung growth were examined in weanling (22-day-old) and suckling (5-day-old) rats infected with parainfluenza Type 1 (Sendai) virus. Viral nucleocapsids and budding virions were identified by transmission electron microscopy in ciliated cells, mucous cells, and nonciliated bronchiolar epithelial cells of weanling rats at 5 days after inoculation and were associated with epithelial necrosis and erosion as well as hyperplasia of nonciliated bronchiolar epithelial cells. Interstitial pneumonia characterized in early stages by swelling and sloughing of Type 1 and Type 2 alveolar epithelial cells was also present at 5 and 7 days after inoculation. Lesions persisting at 30, 60, and 90 days after inoculation included multifocal connective tissue polyps in terminal bronchioles that partially obstructed bronchiolar lumens. Specific lung volume was greater (P less than 0.01) in weanling rats at 30 and 60 days following viral infection than in control rats, and specific alveolar surface area was 42% greater (P less than 0.01) in infected rats at 60 days after inoculation. Suckling rats infected during a phase of rapid postnatal lung growth at 5 days of age had 33% greater (P less than 0.02) specific alveolar surface area and 48% greater (P less than 0.001) mean terminal bronchiolar cross-sectional area when compared with control rats at 22 days of age. The results indicate that viral pulmonary infection during early life can induce acute and persistent alterations in pulmonary structure that could adversely affect lung function.
在出生后肺生长期间，对感染1型副流感病毒（仙台病毒）的断奶（22日龄）和哺乳（5日龄）大鼠，检查了病毒性呼吸道疾病的超微结构和形态测量学影响。接种后5天，在断奶大鼠的纤毛细胞、黏液细胞和无纤毛细支气管上皮细胞中，通过透射电子显微镜鉴定出病毒核衣壳和出芽病毒粒子，它们与上皮坏死、糜烂以及无纤毛细支气管上皮细胞增生有关。接种后5天和7天，还出现了间质性肺炎，早期表现为1型和2型肺泡上皮细胞肿胀和脱落。接种后30、60和90天持续存在的病变包括终末细支气管中的多灶性结缔组织息肉，这些息肉部分阻塞了细支气管腔。病毒感染后30天和60天，断奶大鼠的比肺体积比对照大鼠大（P<0.01），接种后60天，感染大鼠的比肺泡表面积比对照大鼠大42%（P<0.01）。在出生后肺快速生长阶段5日龄时感染的哺乳大鼠，与22日龄的对照大鼠相比，比肺泡表面积大33%（P<0.02），平均终末细支气管横截面积大48%（P<0.001）。结果表明，生命早期的病毒性肺部感染可引起肺部结构的急性和持续性改变，这可能对肺功能产生不利影响。
