摘要
目的建立幽门螺杆菌（Hp）感染慢性阻塞性肺病（COPD）大鼠模型，探讨Hp感染在COPD进展中的作用机制。方法40只Wistar大鼠均分为双重造模组（Hp感染、烟熏、气管内滴入脂多糖）、COPD组（烟熏、气管内滴入脂多糖）、Hp感染组及对照组。检测各组大鼠肺功能、血清及支气管肺泡灌洗液中细胞因子、支气管肺组织Hp相关基因表达水平，并进行支气管肺组织Hp分离培养。结果COPD组和双重造模组大鼠肺组织均符合COPD病理表现，且后者病理改变更为明显。COPD组、双重造模组大鼠肺功能均较对照组及Hp感染组显著下降（P值均〈0．05），且双重造模组肺功能改变较COPD组更为明显（P值均〈0．05）。随胃内Hp定植密度增加，双重造模组大鼠吸气阻力、呼气阻力上升（r值分别-0．785和0．905），动态肺顺应性、呼气峰值流速、0．3s呼气容积占肺活量的比例下降（r值分别=-0．975、-0．959、-0．976）。与对照组比较，其余各组大鼠血清及支气管肺泡灌洗液中细胞因子IL-6、IL-8、肿瘤坏死因子（TNF）-α水平均显著升高（P值均〈0．05），其中双重造模组升高最明显（P值均〈0．05）。仅部分双重造模组大鼠支气管肺组织中扩增出Hp尿素酶相关蛋白（UreC）基因，各组均未分离培养出Hp及可疑菌落。结论Hp不直接定植于支气管肺组织，而是通过提高COPD模型大鼠血清及支气管肺泡中细胞因子水平而加重炎性反应，并由此导致COPD模型大鼠肺功能恶化。
Objective To establish Helicobacter pylori （Hp） infection induced chronic obstructive pulmonary disease （COPD） rat model, and to explore the role of Hp in the pathogenesis of COPD. Methods 40 Wistar rats were randomly divided into double modeling group （Hp infection, smoked and intratracheal instillation of lipopolysaccharide）, COPD group （smoked and intratracheal instillation of lipopolysaccharide）, Hp infected group and control group. The lung funct!on, cytokines level in serum and bronchial alveolar lavage fluid （BALF）, Hp related genes expression in bronchial and lung tissue were detected. And Hp in bronchial and lung tissue was isolated and cultured. Results The lung tissue of both COPD group and double modeling group accorded with COPD pathological characteristics, and the latter was more apparent. The lung function of COPD group and double modeling group decreased more significantly than that of control group and Hp infected group （all P〈 0.05）, and which was more obvious in double modeling group than that of COPD group （P〈0.05）. Along with the Hp colonization density increased, Ri and Re value of double modeling group increased （r=0. 785 and 0. 905）, the value of Gdyn, PEF and FEV0.3/FVC decreased （r= -0. 975, -0. 959 and -0. 976）. Compared with control group, IL-6, IL-8 and TNF-α cytokines levels in serum and bronchoalveolar lavage fluid of other groups increased significantly （all P〈 0. 05）, and within the groups, double modeling group increased most significantly （all P〈0.05）. Hp UreC gene was only amplified in part of bronchi and lung tissue of double modeling group, no Hp and suspicious bacteria colonies were isolated and cultured. Conclusions Hp not directly colonized in bronchi and lung tissue, which aggravated inflammation through increasing the serum and bronchoalveolar cytokines level of COPD rat model. Which caused the deterioration in lung function of COPD group.
出处
《中华消化杂志》
CAS
CSCD
北大核心
2011年第11期757-760,共4页
Chinese Journal of Digestion
关键词
幽门螺杆菌
疾病模型
动物
慢性阻塞性肺疾病
细胞因子类
Helicobacter pylori Disease models, animal
Chronic obstructive pulmonary disease Cytokines
