水通道蛋白4和P65在肠道病毒71型感染合并神经源性肺水肿死亡病例中的研究
发布时间：2019-02-14 16:13
【摘要】：目的:通过检测AQP4及P65在肠道病毒71型(EV71)感染合并神经源性肺水肿(NPE)死亡病例肺和脑组织中的表达,探讨二者的表达在神经源性肺水肿发病中的意义。方法:收集10例桂林地区7家医院于2010年3月-2014年6月收治的手足口病(经病原学检测均为肠道病毒EV71感染)合并肺水肿死亡病例,同期收集10例桂林市5家医院收治的非EV71感染间质性肺炎并发肺水肿死亡病例。分组:以10例EV71感染合并肺水肿(PE)死亡病例为研究对象(PE组),以同期10例非EV71感染合并肺水肿死亡病例为对照组。本实验提取了石蜡包埋的肺、脑组织标本,行病理切片(4μm),进行病理组织学检查。对死亡病例肺、脑组织进行HE染色,镜下观察组织病理变化。采用免疫组织化学方法对AQP4及P65在两组病例肺、脑组织的表达进行定性检测,采用积分光密度值(IOD)对AQP4及P65进行半定量检测。结果:组织大体外观:(1)肺组织:PE组及对照组两肺表面、切面见片状暗红淤血或出血,肺叶肺血管扩张淤血、肺泡腔内充满粉红色水肿液。(2)脑组织:PE组脑组织见脑沟变浅,脑回增宽,多切面未见出血及肿瘤,而对照组脑实质内未见明显水肿、软化灶及出血灶。HE染色镜下组织病理改变:(1)肺组织:PE组及对照组肺间质可见毛细血管明显扩张、充血,部分肺泡间隔增宽,较多炎性细胞呈灶性浸润,部分肺泡腔内积满红细胞及粉红色水肿液。(2)脑组织:PE组脑组织可见神经元变性、坏死,形成噬神经现象,小胶质细胞吞噬炎性细胞形成胶质结节,炎性细胞围绕小血管周围形成袖套状浸润;但对照组脑组织未见噬神经现象及炎性细胞浸润。免疫组化结果示:(1)AQP4在PE组及对照组肺组织均呈阳性表达,在PE组肺组织检测到强阳性表达信号,对照组肺组织检测到中度阳性表达信号,两者IOD值比较差异有统计学意义(P0.05);AQP4在PE组及对照组脑组织中的表达:PE组脑组织检测到中度阳性表达信号,对照组脑组织检测到弱阳性表达信号,两者IOD值比较差异有统计学意义(P0.01)。(2)P65在PE组肺组织检测到强阳性信号表达,在对照组肺组织呈阳性信号表达;P65 IOD值在两组肺组织间比较差异有统计学意义(P0.05);P65在PE组脑组织呈强阳性表达,在对照组脑组织呈较弱阳性表达,两者IOD值比较差异有统计学意义(P0.01)。(3)P65和AQP4在PE组肺组织均检测到强阳性信号表达,两者IOD值比较差异有统计学意义(P0.05);P65及AQP4在对照组肺组织检测到中度阳性信号表达,两者IOD值比较差异有统计学意义(P0.01)。(4)P65和AQP4在PE组脑组织信号表达均呈阳性,两者IOD值比较差异有统计学意义(P0.05);P65及AQP4在对照组脑组织检测到弱阳性信号表达,两者IOD值比较差异有统计学意义(P0.01)。结论:AQP4及P65在EV71感染合并神经源性肺水肿死亡病例脑与肺组织中检测到高表达信号,提示AQP4和P65可能参与了EV71致神经源性肺水肿的形成。
[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.
【学位授予单位】：桂林医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R725.1
本文编号：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.
【学位授予单位】：桂林医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R725.1
【参考文献】
相关期刊论文 前5条
1 陈洁;娄洁婵;李素华;陈均亚;徐志伟;陈喻;陈益平;;肠道病毒71型感染患儿血清内皮素-1的变化与疾病预后关系研究[J];中华医院感染学杂志;2015年15期
2 高媛媛;陶建平;刘鸿圣;宁书尧;杨思达;;手足口病相关性肺渗出性改变与脑干受累的关系[J];广东医学;2013年23期
3 郑伟华;杨方源;李雄;李运千;欧维琳;;肠道病毒71型感染9例临床及尸体解剖特点[J];实用儿科临床杂志;2012年10期
4 朱丽华;李涛平;何琳;;大鼠油酸性急性肺损伤初期水通道蛋白4在肺水代谢的实验研究[J];南方医科大学学报;2008年05期
5 王纪文;薛宁;孙若鹏;;肠道病毒71型感染的神经系统表现及其心肺衰竭的发生机制[J];中华儿科杂志;2009年08期
，本文编号：2422374
本文链接：https://www.wllwen.com/yixuelunwen/eklw/2422374.html
最近更新
教材专著
