鸭霍乱的肺损伤组织病理学观察及肺水肿相关基因的表达

发布时间：2018-07-11 10:53

本文选题：鸭 + 多杀性巴氏杆菌　；参考：《华中农业大学》2015年硕士论文

【摘要】：多杀性巴氏杆菌(Pasteurella multocida)是一种在世界范围内广泛引起人和多种动物发病的致病菌,可导致急性、败血性传染病。鸭巴氏杆菌病又称鸭霍乱、鸭出血性败血症,该病发病急,传染性强,死亡率高,具有严重危害。鸭霍乱的主要临床症状为呼吸困难,频频摇头或转圈,剧烈腹泻,排出黄绿色稀粪等。大部分病例中,肺脏病变较为普遍,主要为肺充血、出血及肺水肿。肺水肿可以由肺泡上皮屏障功能损伤和肺泡毛细血管通透性增高引发,而肾素-血管紧张素系统(RAS)中的主要效应分子血管紧张素II(AngII)能诱导上述损伤,并通过激活MAPK信号通路和NF-κB信号通路介导机体产生炎症。同时,有研究表明水通道蛋白(aquaporin,AQP)家族中的AQP1和AQP5与肺水肿关系密切。为了了解多杀性巴氏杆菌致鸭肺水肿的机制,本试验以多杀性巴氏杆菌感染30日龄鸭为研究对象,通过病理学技术和荧光定量PCR技术,分析感染后4h、12h、24h、36h、48h鸭肺部病理变化,检测AQP1、AQP5、AT1R(血管紧张素II受体1,angiotensin II type 1 receptor)和TNF-αm RNA水平表达量的变化,评价组织学病变与各指标变化的关系。结果表明:⑴多杀性巴氏杆菌可以引起鸭肺出现明显的水肿、淤血、出血病变。感染后4h-48h,组织学变化为肺小叶间隔增宽,三级支气管、肺房、肺间质有浆液渗出,肺组织间炎性细胞浸润,肺房和呼吸毛细管严重出血,小叶间静脉充血。⑵肺组织AT1R mRNA的表达感染后4h-36h上调,48h表达量下调,与对照组相比差异不显著(P0.05);AQP1 mRNA的表达量在感染后下调,与对照组相比差异不显著(P0.05);AQP5mRNA的表达量在感染后4h、12h、36h、48h下调,在24h上调,但与对照组相比差异不显著(P0.05);TNF-αmRNA的表达量在感染后4h-36h均上调,48h下调,与对照组相比差异不显著(P0.05)。本试验首次明确了鸭肺部表达AQP1、AQP5和AT1R,证明鸭肺部存在局部RAS系统。感染P.multocida鸭肺组织中AQP1和AQP5 mRNA水平表达量下降,AT1R和TNF-αmRNA水平表达量升高,而组织学病变显示各个时间点均出现浆液渗出,肺小叶间距增宽,说明肺内血气屏障出现损伤,液体平衡被破坏进而形成淤血和水肿,可以推测AQP1、AQP5的下调、AT1R的上调与P.multocida感染引起的鸭肺水肿有相关性。
[Abstract]:Pasteurella multocida (Pasteurella multocida) is a kind of pathogenic bacteria which causes human and many animal diseases in the world, and can cause acute, septic infectious disease. Duck pasteulosis, also known as duck cholera, is an acute, infectious disease with high mortality and is a serious hazard to hemorrhagic septicemia in ducks. The main clinical symptoms of duck cholera are dyspnea, shaking head or circle frequently, severe diarrhea, excretion of yellowish green feces and so on. In most cases, pulmonary lesions are common, mainly hyperemia, hemorrhage and pulmonary edema. Pulmonary edema can be induced by alveolar epithelial barrier dysfunction and increased alveolar capillary permeability, which is induced by angiotensin II (AngII), a major effector molecule in the renin-angiotensin system (Ras). Inflammation is mediated by activation of MAPK and NF- 魏 B signaling pathways. At the same time, some studies have shown that AQP1 and AQP5 in aquaporin (AQP) family are closely related to pulmonary edema. In order to understand the mechanism of pulmonary edema induced by Pasteurella multocida, the lung pathological changes of ducks at 30 days old infected by Pasteurella multocida were analyzed by pathological technique and fluorescence quantitative PCR (FQ-PCR). The expression of AT1R (angiotensin II type 1 receptor) and TNF- 伪 mRNA were detected in AQP1, AQP5 and AT1R (angiotensin II type 1 receptor). The results showed that Pasteurella multocida caused obvious edema, congestion and hemorrhage in duck lung. At 4h-48h after infection, the histological changes were as follows: pulmonary lobular septal widening, serous exudation of third stage bronchi, pulmonary atrium, pulmonary interstitium, infiltration of inflammatory cells between lung tissues, severe hemorrhage of pulmonary atrium and respiratory capillaries. The expression of AT1R mRNA in pulmonary tissue was up-regulated and down-regulated by 4h-36h at 48h after infection, but there was no significant difference compared with the control group (P0.05). The expression of AT1R mRNA in pulmonary tissue was down-regulated after infection (P0.05). Compared with the control group, there was no significant difference (P0.05) in the expression of AQP5 mRNA. The expression of AQP5 mRNA was down-regulated at 4h, 12h, 36h, 48h and 24h, but there was no significant difference compared with the control group (P0.05). The expression of TNF- 伪 mRNA was down-regulated at 48h after 4h-36h infection, but not significantly compared with the control group (P0.05). The expression of AQP1AAQP5 and AT1R in duck lung was confirmed for the first time, which proved that there was a local Ras system in duck lung. The expression of AQP1 and AQP5 mRNA in the lung tissues of P. multocida infected duck decreased and the expression of AT1R and TNF- 伪 mRNA increased. The histological changes showed that serous exudation and pulmonary lobular spacing were observed at all time points, which indicated that the blood gas barrier in the lung was damaged. The fluid balance was destroyed and blood stasis and edema were formed. It can be inferred that the down-regulation of AT1R in AQP1 was correlated with pulmonary edema induced by P. multocida infection in ducks.
【学位授予单位】：华中农业大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：S858.32

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