Slater E, Owen R J, Williams M, Pounder R E
Laboratory of Enteric Pathogens, Central Public Health Laboratory, London, England.
Gastroenterology. 1999 Dec;117(6):1308-15. doi: 10.1016/s0016-5085(99)70281-7.
BACKGROUND & AIMS: Specific regions of the cag pathogenicity island (PAI) believed to enhance the virulence of Helicobacter pylori, as well as vacuolating cytotoxin gene alleles and IS605 inserts, were investigated to define diversity within infecting strain populations from patients with peptic ulcer disease and from healthy individuals.
The H. pylori studied comprised 67 isolates from 26 subjects and 14 reference strains. Specific polymerase chain reaction assays were used to test for cagA and picB in the cagI region, the virD4 homologue in the cagII region, IS605 in the genome and in the cag PAI, the "empty site" indicating absence of the cag PAI, and different vacA gene alleles.
Most (89%) subjects were infected by H. pylori with a contiguous cag PAI. No intermediate forms were found. IS605 was not detected within the cag PAI of any strain but was present elsewhere in the genomes of strains from 62% of subjects. Twenty individuals were infected with genotypically conserved populations of H. pylori. Six subjects had mixed infections, and in 3 of these cag(+)/cag(-) variants were present.
The cag PAI-positive H. pylori was a feature of most infected individuals, irrespective of severity of associated disease. Combined genotyping showed that 8 individuals (31%) had mixed infections, which suggests that strain population structure may be an additional contributing factor in disease development.
研究了空泡毒素致病岛(PAI)中被认为可增强幽门螺杆菌毒力的特定区域,以及空泡毒素基因等位基因和IS605插入序列,以确定消化性溃疡疾病患者和健康个体感染菌株群体的多样性。
所研究的幽门螺杆菌包括来自26名受试者的67株分离株和14株参考菌株。采用特异性聚合酶链反应检测cagI区域中的cagA和picB、cagII区域中的virD4同源物、基因组和cag PAI中的IS605、表明不存在cag PAI的“空位”以及不同的vacA基因等位基因。
大多数(89%)受试者感染的幽门螺杆菌具有连续的cag PAI。未发现中间形式。在任何菌株的cag PAI中均未检测到IS605,但在62%受试者的菌株基因组其他位置存在。20名个体感染了基因保守的幽门螺杆菌群体。6名受试者有混合感染,其中3名存在cag(+)/cag(-)变体。
cag PAI阳性的幽门螺杆菌是大多数感染者的特征,与相关疾病的严重程度无关。联合基因分型显示8名个体(31%)有混合感染,这表明菌株群体结构可能是疾病发展的另一个促成因素。