慢性肺部炎症合并肺炎支原体肺炎小鼠模型的建立

目的肺炎支原体肺炎(MPP)是肺炎支原体(MP)引起的以肺间质纤维结缔组织增生为主要病理改变的间质性肺炎。在临床易感于慢性肺部炎症病人,基于此原因本研究使用烟熏并肺炎支原体感染方法建立慢性肺部炎症合并肺炎支原体肺炎实验动物模型。方法本研究采用Realtime PCR、HE和Masson染色方法观察小鼠感染前后肺部肺炎支原体浓度、肺组织病变状况和肺组织胶原纤维生成情况。结果烟熏并感染组小鼠肺炎支原体感染率达到93%,肺泡腔塌陷,肺组织呈片状致密结构,内充斥大量红细胞,胶原纤维增多呈片状蓝染。结论通过实验可知烟熏并感染组小鼠肺内支原体浓度增高、肺组织病变情况严重,胶原纤维生成增多,预示慢性肺部炎症合并肺炎支原体间质性肺炎模型建立成功。

Establishment of Experimental Animal Model of Chronic Pulmonary Inflammation Combined with Mycoplasma Pneumoniae Pneumonia

Objective Mycoplasma pneumoniae pneumonia ( MPP ) is an interstitial pneumonia caused by Mycoplasma pneumoniae ( MP ) with fibrous connective tissue hyperplasia in the pulmonary interstitial as the main pathological change , in clinically susceptible patients with chronic lung inflammation. For this reason , the study used a method of smoking and Mycoplasma pneumoniae infection to establish an experimental animal model of Mycoplasma pneumoniae interstitial pneumonia. Method Realtime PCR , HE and Masson staining were used to observe the concentration of Mycoplasma pneumoniae and the deposition of cellulose in lung tissue after infection in mice. Result In the smoked and infected group, the infection rate of Mycoplasma pneumoniae was 93%, the alveolar cavity collapsed , a flaky dense structure in the lung tissue , and thered blood cells filled with alarge amount of cellulose. Conclusion The lung tissue lesions of the smoked and infected mice are severe , showing a state of cellulose deposition .The model of chronic lung inflammation combined with Mycoplasma pneumoniae interstitial pneumonia was successfully established.