Kim Hyun-Soo, DO Sung-Im, Kim Youn Wha
Department of Pathology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 135-710, Republic of Korea ; Republic of Korea Air Force Aerospace Medical Center, Chungcheongbuk-do 363-849, Republic of Korea.
Department of Pathology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul 110-746, Republic of Korea.
Exp Ther Med. 2014 Aug;8(2):442-446. doi: 10.3892/etm.2014.1732. Epub 2014 May 26.
The occurrence of idiopathic pulmonary lesions in laboratory rats, characterized by lymphohistiocytic interstitial pneumonia with dense perivascular lymphoid cuffs, has been reported over the past decade. Although the term rat respiratory virus (RRV) was adopted to confer a putative viral etiology to the idiopathic pulmonary lesions, the etiology of this disease remains to be elucidated. Recently, inflammatory lesions have been observed in the lungs of immunocompetent laboratory rats similar to those previously described. Based on the latest evidence indicating that , and not putative RRV, causes infectious interstitial pneumonia in laboratory rats, the present study investigated whether the pulmonary lesions observed were caused by infection. Male Sprague-Dawley rats, free of known pathogens, were introduced into a rat colony positive for RRV-type lesions. Routine histopathological examinations were performed on the rat lung tissues following exposure. The presence of organisms was confirmed using Grocott's methenamine silver (GMS) staining. At week 3 following introduction, a few small lymphoid aggregates were located adjacent to the edematous vascular sheath. By week 5, foci of dense perivascular lymphoid cuffing were observed. Multifocal lymphohistiocytic interstitial pneumonia and prominent lymphoid perivascular cuffs were observed between week 7 and 10. GMS staining confirmed the presence of cysts. Thus, the results of the present study demonstrated that caused lymphohistiocytic interstitial pneumonia in a group of laboratory rats. The observations strongly support the conclusion that infection in immunocompetent laboratory rats causes the lung lesions that were previously attributed to RRV.
在过去十年中，已报道实验大鼠出现特发性肺部病变，其特征为淋巴细胞性间质性肺炎伴致密的血管周围淋巴细胞套。尽管采用了大鼠呼吸道病毒（RRV）这一术语来赋予特发性肺部病变一种假定的病毒病因，但该疾病的病因仍有待阐明。最近，在免疫功能正常的实验大鼠肺部观察到了与先前描述相似的炎症性病变。基于最新证据表明，是[具体病原体名称未给出]而非假定的RRV导致实验大鼠发生感染性间质性肺炎，本研究调查了观察到的肺部病变是否由[具体病原体名称未给出]感染引起。将无已知病原体的雄性Sprague-Dawley大鼠引入RRV型病变呈阳性的大鼠群体中。暴露后对大鼠肺组织进行常规组织病理学检查。使用Grocott六胺银（GMS）染色确认[具体病原体名称未给出]生物体的存在。引入后第3周，在水肿的血管鞘附近有一些小的淋巴聚集物。到第5周时，观察到致密的血管周围淋巴细胞套灶。在第7至10周期间观察到多灶性淋巴细胞性间质性肺炎和显著的血管周围淋巴细胞套。GMS染色证实存在[具体病原体名称未给出]囊肿。因此，本研究结果表明[具体病原体名称未给出]在一组实验大鼠中引起了淋巴细胞性间质性肺炎。这些观察结果有力地支持了以下结论：免疫功能正常的实验大鼠中的[具体病原体名称未给出]感染导致了先前归因于RRV的肺部病变。
