水通道蛋白4和P65在腸道病毒71型感染合并神經(jīng)源性肺水腫死亡病例中的研究
發(fā)布時(shí)間：2019-02-14 16:13
【摘要】：目的:通過檢測(cè)AQP4及P65在腸道病毒71型(EV71)感染合并神經(jīng)源性肺水腫(NPE)死亡病例肺和腦組織中的表達(dá),探討二者的表達(dá)在神經(jīng)源性肺水腫發(fā)病中的意義。方法:收集10例桂林地區(qū)7家醫(yī)院于2010年3月-2014年6月收治的手足口病(經(jīng)病原學(xué)檢測(cè)均為腸道病毒EV71感染)合并肺水腫死亡病例,同期收集10例桂林市5家醫(yī)院收治的非EV71感染間質(zhì)性肺炎并發(fā)肺水腫死亡病例。分組:以10例EV71感染合并肺水腫(PE)死亡病例為研究對(duì)象(PE組),以同期10例非EV71感染合并肺水腫死亡病例為對(duì)照組。本實(shí)驗(yàn)提取了石蠟包埋的肺、腦組織標(biāo)本,行病理切片(4μm),進(jìn)行病理組織學(xué)檢查。對(duì)死亡病例肺、腦組織進(jìn)行HE染色,鏡下觀察組織病理變化。采用免疫組織化學(xué)方法對(duì)AQP4及P65在兩組病例肺、腦組織的表達(dá)進(jìn)行定性檢測(cè),采用積分光密度值(IOD)對(duì)AQP4及P65進(jìn)行半定量檢測(cè)。結(jié)果:組織大體外觀:(1)肺組織:PE組及對(duì)照組兩肺表面、切面見片狀暗紅淤血或出血,肺葉肺血管擴(kuò)張淤血、肺泡腔內(nèi)充滿粉紅色水腫液。(2)腦組織:PE組腦組織見腦溝變淺,腦回增寬,多切面未見出血及腫瘤,而對(duì)照組腦實(shí)質(zhì)內(nèi)未見明顯水腫、軟化灶及出血灶。HE染色鏡下組織病理改變:(1)肺組織:PE組及對(duì)照組肺間質(zhì)可見毛細(xì)血管明顯擴(kuò)張、充血,部分肺泡間隔增寬,較多炎性細(xì)胞呈灶性浸潤,部分肺泡腔內(nèi)積滿紅細(xì)胞及粉紅色水腫液。(2)腦組織:PE組腦組織可見神經(jīng)元變性、壞死,形成噬神經(jīng)現(xiàn)象,小膠質(zhì)細(xì)胞吞噬炎性細(xì)胞形成膠質(zhì)結(jié)節(jié),炎性細(xì)胞圍繞小血管周圍形成袖套狀浸潤;但對(duì)照組腦組織未見噬神經(jīng)現(xiàn)象及炎性細(xì)胞浸潤。免疫組化結(jié)果示:(1)AQP4在PE組及對(duì)照組肺組織均呈陽性表達(dá),在PE組肺組織檢測(cè)到強(qiáng)陽性表達(dá)信號(hào),對(duì)照組肺組織檢測(cè)到中度陽性表達(dá)信號(hào),兩者IOD值比較差異有統(tǒng)計(jì)學(xué)意義(P0.05);AQP4在PE組及對(duì)照組腦組織中的表達(dá):PE組腦組織檢測(cè)到中度陽性表達(dá)信號(hào),對(duì)照組腦組織檢測(cè)到弱陽性表達(dá)信號(hào),兩者IOD值比較差異有統(tǒng)計(jì)學(xué)意義(P0.01)。(2)P65在PE組肺組織檢測(cè)到強(qiáng)陽性信號(hào)表達(dá),在對(duì)照組肺組織呈陽性信號(hào)表達(dá);P65 IOD值在兩組肺組織間比較差異有統(tǒng)計(jì)學(xué)意義(P0.05);P65在PE組腦組織呈強(qiáng)陽性表達(dá),在對(duì)照組腦組織呈較弱陽性表達(dá),兩者IOD值比較差異有統(tǒng)計(jì)學(xué)意義(P0.01)。(3)P65和AQP4在PE組肺組織均檢測(cè)到強(qiáng)陽性信號(hào)表達(dá),兩者IOD值比較差異有統(tǒng)計(jì)學(xué)意義(P0.05);P65及AQP4在對(duì)照組肺組織檢測(cè)到中度陽性信號(hào)表達(dá),兩者IOD值比較差異有統(tǒng)計(jì)學(xué)意義(P0.01)。(4)P65和AQP4在PE組腦組織信號(hào)表達(dá)均呈陽性,兩者IOD值比較差異有統(tǒng)計(jì)學(xué)意義(P0.05);P65及AQP4在對(duì)照組腦組織檢測(cè)到弱陽性信號(hào)表達(dá),兩者IOD值比較差異有統(tǒng)計(jì)學(xué)意義(P0.01)。結(jié)論:AQP4及P65在EV71感染合并神經(jīng)源性肺水腫死亡病例腦與肺組織中檢測(cè)到高表達(dá)信號(hào),提示AQP4和P65可能參與了EV71致神經(jīng)源性肺水腫的形成。
[Abstract]:Objective: to investigate the expression of AQP4 and p65 in lung and brain tissues of patients with (NPE) death caused by enterovirus 71 (EV71) infection and neurogenic pulmonary edema, and to explore their significance in the pathogenesis of neurogenic pulmonary edema. Methods: ten cases of hand, foot and mouth disease (enterovirus EV71 infection) with pulmonary edema were collected from 7 hospitals in Guilin from March 2010 to June 2014. Ten cases of non-EV71 infected interstitial pneumonia with pulmonary edema death were collected from 5 hospitals in Guilin. Group: ten cases of EV71 infection with pulmonary edema (PE) death (PE group) and 10 cases of non-EV71 infection with pulmonary edema death case as control group. The paraffin embedded lung and brain specimens were extracted and examined by histopathology (4 渭 m),). Lung and brain tissues were stained with HE and histopathological changes were observed under microscope. The expression of AQP4 and p65 in lung and brain tissues were detected qualitatively by immunohistochemical method, and AQP4 and p65 were detected semi-quantitatively by integral optical density value (IOD). Results: (1) Lung tissue: (1) Pulmonary tissue: in PE group and control group, there were flake dark red congestion or hemorrhage on the surface of lung, and pulmonary vascular dilatation and congestion in lobar lung. The alveolar cavity was filled with pink edema fluid. (2) brain tissue: in the PE group, the sulcus was shallower, the gyrus widened, there was no hemorrhage or tumor on multiple sections, but there was no obvious edema in the brain parenchyma in the control group. The pathological changes under HE staining were as follows: (1) Pulmonary tissue: in PE group and control group, capillary dilation and hyperemia were observed, and some alveolar septum were enlarged and more inflammatory cells were infiltrated. Part of alveolar cavity was filled with red blood cells and pink edema fluid. (2) brain tissue: neurons degeneration, necrosis, phagocytosis of microglia and inflammatory cells formed glial nodules in PE group. The inflammatory cells formed cuff infiltration around the small vessels. However, no macrophage and inflammatory cell infiltration were found in the brain of the control group. The results of immunohistochemistry showed that: (1) the positive expression of AQP4 was detected in the lung tissues of PE group and control group, the strong positive signal was detected in the lung tissue of PE group, and the moderate positive signal was detected in the lung tissue of control group. The difference of IOD between the two groups was statistically significant (P0.05). Expression of AQP4 in brain tissue of PE group and control group: moderate positive signal was detected in brain tissue of PE group and weak positive signal was detected in brain tissue of control group. There was a significant difference in IOD between the two groups (P0.01). (2) p65 was detected in the lung tissue of PE group, and positive signal expression was found in the lung tissue of the control group. There was significant difference in p65 IOD between the two groups (P0.05). The expression of p65 was strongly positive in brain tissue of PE group and weakly positive in brain tissue of control group. There was a significant difference in IOD between the two groups (P0.01). (3) strong positive signal expression of p65 and AQP4 was detected in lung tissue of PE group. The difference of IOD between the two groups was statistically significant (P0.05). Moderate positive signal expression of p65 and AQP4 was detected in lung tissue of control group. The difference of IOD value between them was statistically significant (P0.01). (4) P65 and AQP4 were positive in brain tissue of PE group. The difference of IOD between the two groups was statistically significant (P0.05). Weak positive signal expression of p65 and AQP4 was detected in brain tissue of control group, the difference of IOD between them was statistically significant (P0.01). Conclusion: high expression of AQP4 and p65 were detected in brain and lung tissues of patients with EV71 infection and death of neurogenic pulmonary edema, suggesting that AQP4 and p65 may be involved in the formation of EV71 induced neurogenic pulmonary edema.
【學(xué)位授予單位】：桂林醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R725.1
本文編號(hào)：2422374
[Abstract]:Objective: to investigate the expression of AQP4 and p65 in lung and brain tissues of patients with (NPE) death caused by enterovirus 71 (EV71) infection and neurogenic pulmonary edema, and to explore their significance in the pathogenesis of neurogenic pulmonary edema. Methods: ten cases of hand, foot and mouth disease (enterovirus EV71 infection) with pulmonary edema were collected from 7 hospitals in Guilin from March 2010 to June 2014. Ten cases of non-EV71 infected interstitial pneumonia with pulmonary edema death were collected from 5 hospitals in Guilin. Group: ten cases of EV71 infection with pulmonary edema (PE) death (PE group) and 10 cases of non-EV71 infection with pulmonary edema death case as control group. The paraffin embedded lung and brain specimens were extracted and examined by histopathology (4 渭 m),). Lung and brain tissues were stained with HE and histopathological changes were observed under microscope. The expression of AQP4 and p65 in lung and brain tissues were detected qualitatively by immunohistochemical method, and AQP4 and p65 were detected semi-quantitatively by integral optical density value (IOD). Results: (1) Lung tissue: (1) Pulmonary tissue: in PE group and control group, there were flake dark red congestion or hemorrhage on the surface of lung, and pulmonary vascular dilatation and congestion in lobar lung. The alveolar cavity was filled with pink edema fluid. (2) brain tissue: in the PE group, the sulcus was shallower, the gyrus widened, there was no hemorrhage or tumor on multiple sections, but there was no obvious edema in the brain parenchyma in the control group. The pathological changes under HE staining were as follows: (1) Pulmonary tissue: in PE group and control group, capillary dilation and hyperemia were observed, and some alveolar septum were enlarged and more inflammatory cells were infiltrated. Part of alveolar cavity was filled with red blood cells and pink edema fluid. (2) brain tissue: neurons degeneration, necrosis, phagocytosis of microglia and inflammatory cells formed glial nodules in PE group. The inflammatory cells formed cuff infiltration around the small vessels. However, no macrophage and inflammatory cell infiltration were found in the brain of the control group. The results of immunohistochemistry showed that: (1) the positive expression of AQP4 was detected in the lung tissues of PE group and control group, the strong positive signal was detected in the lung tissue of PE group, and the moderate positive signal was detected in the lung tissue of control group. The difference of IOD between the two groups was statistically significant (P0.05). Expression of AQP4 in brain tissue of PE group and control group: moderate positive signal was detected in brain tissue of PE group and weak positive signal was detected in brain tissue of control group. There was a significant difference in IOD between the two groups (P0.01). (2) p65 was detected in the lung tissue of PE group, and positive signal expression was found in the lung tissue of the control group. There was significant difference in p65 IOD between the two groups (P0.05). The expression of p65 was strongly positive in brain tissue of PE group and weakly positive in brain tissue of control group. There was a significant difference in IOD between the two groups (P0.01). (3) strong positive signal expression of p65 and AQP4 was detected in lung tissue of PE group. The difference of IOD between the two groups was statistically significant (P0.05). Moderate positive signal expression of p65 and AQP4 was detected in lung tissue of control group. The difference of IOD value between them was statistically significant (P0.01). (4) P65 and AQP4 were positive in brain tissue of PE group. The difference of IOD between the two groups was statistically significant (P0.05). Weak positive signal expression of p65 and AQP4 was detected in brain tissue of control group, the difference of IOD between them was statistically significant (P0.01). Conclusion: high expression of AQP4 and p65 were detected in brain and lung tissues of patients with EV71 infection and death of neurogenic pulmonary edema, suggesting that AQP4 and p65 may be involved in the formation of EV71 induced neurogenic pulmonary edema.
【學(xué)位授予單位】：桂林醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R725.1
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