卡氏肺孢子菌肺炎动物模型建立及其病原体的超微结构观察

Establishment of pneumonia model for pneumocystis carinii and observation of its′ ultra-structure in rat

目的建立SD大鼠的卡氏肺孢子菌肺炎(PCP)的实验动物模型,观察肺组织病理变化特点和卡氏肺孢子菌(Pc)的超微结构特征,探讨其致病机制。方法地塞米松皮下注射诱导SD大鼠PCP,肺印片吉姆萨染色检测Pc滋养体,GMS染色检测Pc包囊,肺组织切片HE染色观察肺组织病理变化,透射电镜观察Pc超微结构。结果地塞米松诱导6周后,大鼠肺印片可见少许Pc滋养体和少许包囊,第9周肺泡腔内可见大量滋养体和包囊;PCP肺泡腔变小,肺泡上皮增生,间隔增宽,肺间质内有以淋巴细胞、嗜酸性粒细胞为主的细胞浸润并伴炎性物质渗出,并随病程时间延长炎症进行性加重;透射电镜显示,Pc黏附在肺Ⅰ型上皮细胞,滋养体形态多样,表面有管状突出和伪足样结构,内部含有丰富的线粒体、内质网、管状小体、囊内小体、高密度特殊颗粒等超微结构;包囊表面有皱褶但未见管状突起,囊内有数个囊内小体,具有滋养体样特征。结论 Pc对肺Ⅰ型上皮细胞的黏附和过度繁殖增生以及刺激肺间质大量炎性细胞浸润和炎性物质渗出是引发PCP不可逆肺损伤的重要因素。

Objective To observe the pathological change of lung tissue and the ultra-structure of p. carinii,P, carinii pneumonia was induced in SD rats using Dexamethasone. Methods The P. carinii was detected by microscope with staining of Giemsa for trophozoites, GMS for cyst and HE staining for lung tissue slice. The ultra-structure of P. earinii was observed by transmission elec tron microscopy. Results A few trophozoites and cysts were found in the alveolar cavity at weeks 6 and more organisms in severe case at weeks 9. It were noted that the shrinken alveolar space, proliferated alveolar epithelium, broadening alveolar septum, num- bers of infiltrating inflammatory cell and rosiness foam-like extravasate in the lung tissue of PCP. Many ultra-structures were oh- served by TEM, such as mitochondria, endoplasmic reticulum, tubular bodies, intracystie bodies, high-density specific granule, and so on. Conclusion The adherency and excessive multiplication of P. carinii, with numbers of infiltrating inflammatory cell and rosiness foam-like exiravasate,ptay a role in the development of inreversible lung lesion in PCP rats.