Maeda S, Yoshida H, Ikenoue T, Ogura K, Kanai F, Kato N, Shiratori Y, Omata M
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan.
Gut. 1999 Mar;44(3):336-41. doi: 10.1136/gut.44.3.336.
cag pathogenicity island (PAI) is reported to be a major virulence factor of Helicobacter pylori.
To characterise cagA and the cag PAI in Japanese H pylori strains.
H pylori isolates from Japanese patients were evaluated for CagA by immunoblot, for cagA transcription by northern blot, and for cagA and 13 other cag PAI genes by Southern blot. cagA negative strains from Western countries were also studied. Induction of interleukin-8 secretion from gastric epithelial cells was also investigated.
All Japanese strains retained cagA. Fifty nine of 63 (94%) strains had all the cag PAI genes. In the remaining four, cag PAI was partially deleted, lacking cagA transcripts and not producing CagA protein. Details of the PAI of these strains were checked; three lacked cagB to cagQ (cagI) and continuously cagS to cag13 (cagII), and the remaining one lacked cagB to cag8. Western cagA negative strains completely lacked cag PAI including cagA. Nucleotide sequence analysis in one strain in which the cag PAI was partially deleted showed that the partial deletion contained 25 kb of cag PAI and the cagA promoter. Interleukin-8 induction was lower with the cag PAI partial deletion strains than with the intact ones. All Japanese cag PAI deleted strains were derived from patients with non-ulcer dyspepsia, whereas 41 of 59 (70%) CagA-producing strains were from patients with peptic ulcers or gastric cancer (p<0.05).
Most Japanese H pylori strains had the intact cag PAI. However, some lacked most of the cag PAI in spite of the presence of cagA. Thus the presence of the cagA gene is not an invariable marker of cag PAI related virulence in Japanese strains.
据报道，细胞毒素相关基因A（cagA）致病岛（PAI）是幽门螺杆菌的主要毒力因子。
对日本幽门螺杆菌菌株中的cagA和cag PAI进行特征分析。
通过免疫印迹法评估来自日本患者的幽门螺杆菌分离株的CagA，通过Northern印迹法评估cagA转录情况，通过Southern印迹法评估cagA和其他13个cag PAI基因。还对来自西方国家的cagA阴性菌株进行了研究。同时研究了胃上皮细胞白细胞介素-8分泌的诱导情况。
所有日本菌株均保留cagA。63株中有59株（94%）具有所有cag PAI基因。其余4株中，cag PAI部分缺失，缺乏cagA转录本且不产生CagA蛋白。检查了这些菌株PAI的详细情况；3株缺乏cagB至cagQ（cagI）以及连续的cagS至cag13（cagII），其余1株缺乏cagB至cag8。西方cagA阴性菌株完全缺乏包括cagA在内的cag PAI。对一株cag PAI部分缺失的菌株进行核苷酸序列分析表明，部分缺失包含25 kb的cag PAI和cagA启动子。cag PAI部分缺失菌株的白细胞介素-8诱导作用低于完整菌株。所有日本cag PAI缺失菌株均来自非溃疡性消化不良患者，而59株产生CagA的菌株中有41株（70%）来自消化性溃疡或胃癌患者（p<0.05）。
大多数日本幽门螺杆菌菌株具有完整的cag PAI。然而，一些菌株尽管存在cagA，但大部分cag PAI缺失。因此，在日本菌株中，cagA基因的存在并非cag PAI相关毒力的恒定标志物。
