Transforming growth factor-beta 1 (TGF-beta1) expression in ovine lentivirus-induced lymphoid interstitial pneumonia

绵羊慢病毒诱导的淋巴间质性肺炎中转化生长因子-β1 (TGF-β1) 的表达

阅读:1

Abstract

The aim of this study was to detect the localization of TGF-beta1 protein expression in normal sheep lungs and lungs with interstitial pneumonia associated with infection with maedi-visna virus (MVV). Immunohistochemical localization of TGF-beta1 was determined in 24 lungs of adult sheep naturally infected with MVV and six control lungs of seronegative sheep. The lungs of infected animals showed different lesional degrees: grade 0, no lesions; grade I, mild; grade II, moderate; grade III, severe. In normal lungs, TGF-beta1 was primarily expressed in airway epithelium, bronchial cartilage and glands, endothelial cells and smooth muscle of blood vessels, alveolar macrophages and type II pneumocytes. No staining was observed in alveolar interstitium. In MVV-infected sheep an increased number of positive alveolar and interstitial macrophages and staining of alveolar interstitium was observed in grade I, grade II and some grade III lesions. In grade III lesions an inverse relationship was found between TGF-beta1 staining and smooth muscle hyperplasia. Small lymphoid aggregates, in general, showed strong reactivity, whereas larger ones showed weak reactivity, mainly associated with follicular areas. No significant differences in the staining intensity of airways and blood vessels were observed between control and MVV lungs. The increased expression of TGF-beta1 in early maedi lesions and its down-regulation in more advanced disease suggest the operation of a temporal regulatory mechanism whereby early expression may lead to the smooth muscle hyperplasia which develops during the disease. The striking inverse relationship between TGF-beta1 expression and follicle organization is intriguing and warrants further investigation.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。