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目的 探讨cag致病岛基因群在中国人感染的幽门螺杆菌 (Hp)中结构特征及其与临床疾病的关系 ,以及根据cag致病岛结构对Hp进行分类的意义。 方法 合成五对针对cagA、cag致病岛中的cagⅠ、cagⅡ、cagⅠ与cagⅡ连接处、及IS 6 0 5等基因片段的引物 ,采用PCR方法分别检测临床分离培养的 10 7株Hp基因中 ,cag致病岛及相关基因结构的存在状态。 结果 cag致病岛总的阳性检出率为95 .3% ,其中cagA、cagⅠ、cagⅡ的阳性率分别为 92 .5 %、86 .9%、6 9.2 % ,在慢性胃炎、消化性溃疡、胃癌等不同疾病组间的检出率差异无显著性 (P >0 .0 5 )。IS 6 0 5的阳性检出率为 43 .9% ,在慢性胃炎中的检出率 (5 2 .2 % )明显高于十二指肠溃疡中的检出率 (13 .6 % ,P <0 .0 5 ) ;cagⅠ与cagⅡ连接处 (呈连续状态存在的cag致病岛 )的检出率仅为 4.7%。其在十二指肠溃疡中的检出率 (14.8% )明显高于慢性胃炎(1.5 % )等 (P <0 .0 1)。cag致病岛阴性的Hp菌株主要来源于慢性胃炎。cagⅠ总的检出率 (86 .9% )明显高于cagⅡ (6 9.2 % ) ,差异在慢性胃炎中有显著性 (P <0 .0 1) ;另外 ,cagⅠ部分片段缺失的中国Hp菌株 ,其中 1株为仅有cagA存在、cagⅡ及cagⅠ其它部分均缺失的Hp ,1株Hp的IS 6 0 5阳性扩增片段明显大于国外标准菌株及?
Objective To investigate the structural characteristics of cag pathogenicity island genome in Helicobacter pylori (Hp) infected by Chinese and its relationship with clinical diseases, and to classify Hp according to the pathogenic island architecture of cag. Methods Five pairs of primers targeting cagⅠ, cagⅡ, cagⅠ and cagⅡ in the cagA and cag pathogenicity island and IS 6 0 5 gene fragments were synthesized. PCR was used to detect 107 Hp genes isolated clinically. cag pathogenicity island and related gene structure of the existence of state. Results The positive rate of cag pathogenicity was 95.3%. The positive rates of cagA, cagⅠ and cagⅡ were 92.5%, 86.9% and 62.2% respectively. In chronic gastritis, peptic ulcer, There were no significant differences in the detection rates of gastric cancer and other disease groups (P> 0.05). The positive detection rate of IS 6 05 was 43.9% and the detection rate in chronic gastritis (52.2%) was significantly higher than that in duodenal ulcer (13.6%, P <0. 05). The detection rate of cagⅠand cagⅡ (cag pathogenicity island in continuous state) was only 4.7%. The detection rate of duodenal ulcer (14.8%) was significantly higher than that of chronic gastritis (1.5%) (P <0.01). Pathogenicity island cag pathogenic Hp strains mainly from chronic gastritis. The overall detection rate of cag Ⅰ (86.9%) was significantly higher than that of cagⅡ (69.2%), and the difference was significant in chronic gastritis (P0.01). In addition, the Chinese Hp strain with partial deletion of cagⅠ, One of them was Hp with cagA only, cagⅡ and other parts of cagⅠ were missing, and the IS 6 0 5 positive amplified fragment of 1 Hp was significantly larger than that of foreign standard strains and?