發(fā)布時(shí)間：2018-07-11 10:53

  本文選題：鴨 + 多殺性巴氏桿菌�。� 參考：《華中農(nóng)業(yè)大學(xué)》2015年碩士論文

【摘要】：多殺性巴氏桿菌(Pasteurella multocida)是一種在世界范圍內(nèi)廣泛引起人和多種動(dòng)物發(fā)病的致病菌,可導(dǎo)致急性、敗血性傳染病。鴨巴氏桿菌病又稱鴨霍亂、鴨出血性敗血癥,該病發(fā)病急,傳染性強(qiáng),死亡率高,具有嚴(yán)重危害。鴨霍亂的主要臨床癥狀為呼吸困難,頻頻搖頭或轉(zhuǎn)圈,劇烈腹瀉,排出黃綠色稀糞等。大部分病例中,肺臟病變較為普遍,主要為肺充血、出血及肺水腫。肺水腫可以由肺泡上皮屏障功能損傷和肺泡毛細(xì)血管通透性增高引發(fā),而腎素-血管緊張素系統(tǒng)(RAS)中的主要效應(yīng)分子血管緊張素II(AngII)能誘導(dǎo)上述損傷,并通過激活MAPK信號(hào)通路和NF-κB信號(hào)通路介導(dǎo)機(jī)體產(chǎn)生炎癥。同時(shí),有研究表明水通道蛋白(aquaporin,AQP)家族中的AQP1和AQP5與肺水腫關(guān)系密切。為了了解多殺性巴氏桿菌致鴨肺水腫的機(jī)制,本試驗(yàn)以多殺性巴氏桿菌感染30日齡鴨為研究對(duì)象,通過病理學(xué)技術(shù)和熒光定量PCR技術(shù),分析感染后4h、12h、24h、36h、48h鴨肺部病理變化,檢測(cè)AQP1、AQP5、AT1R(血管緊張素II受體1,angiotensin II type 1 receptor)和TNF-αm RNA水平表達(dá)量的變化,評(píng)價(jià)組織學(xué)病變與各指標(biāo)變化的關(guān)系。結(jié)果表明:⑴多殺性巴氏桿菌可以引起鴨肺出現(xiàn)明顯的水腫、淤血、出血病變。感染后4h-48h,組織學(xué)變化為肺小葉間隔增寬,三級(jí)支氣管、肺房、肺間質(zhì)有漿液滲出,肺組織間炎性細(xì)胞浸潤(rùn),肺房和呼吸毛細(xì)管嚴(yán)重出血,小葉間靜脈充血。⑵肺組織AT1R mRNA的表達(dá)感染后4h-36h上調(diào),48h表達(dá)量下調(diào),與對(duì)照組相比差異不顯著(P0.05);AQP1 mRNA的表達(dá)量在感染后下調(diào),與對(duì)照組相比差異不顯著(P0.05);AQP5mRNA的表達(dá)量在感染后4h、12h、36h、48h下調(diào),在24h上調(diào),但與對(duì)照組相比差異不顯著(P0.05);TNF-αmRNA的表達(dá)量在感染后4h-36h均上調(diào),48h下調(diào),與對(duì)照組相比差異不顯著(P0.05)。本試驗(yàn)首次明確了鴨肺部表達(dá)AQP1、AQP5和AT1R,證明鴨肺部存在局部RAS系統(tǒng)。感染P.multocida鴨肺組織中AQP1和AQP5 mRNA水平表達(dá)量下降,AT1R和TNF-αmRNA水平表達(dá)量升高,而組織學(xué)病變顯示各個(gè)時(shí)間點(diǎn)均出現(xiàn)漿液滲出,肺小葉間距增寬,說明肺內(nèi)血?dú)馄琳铣霈F(xiàn)損傷,液體平衡被破壞進(jìn)而形成淤血和水腫,可以推測(cè)AQP1、AQP5的下調(diào)、AT1R的上調(diào)與P.multocida感染引起的鴨肺水腫有相關(guān)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- 偽 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- 偽 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- 偽 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.
【學(xué)位授予單位】：華中農(nóng)業(yè)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2015
【分類號(hào)】：S858.32

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