Sheu Shew-Meei, Sheu Bor-Shyang, Yang Hsiao-Bai, Li Ching, Chu Tro-Chen, Wu Jiunn-Jong
Department of Microbiology and Immunology, National Cheng Kung University Medical College, Tainan, Taiwan.
J Formos Med Assoc. 2002 Jan;101(1):18-23.
The presence of the cag pathogenicity island (PAI) may enhance the virulence of Helicobacter pylori. This study determined the prevalence of genotypes of the PAI, IS605, and iceA1 in H. pylori strains in Taiwanese and whether these genotypes were related to the type of clinical disease or gastric pathology.
One hundred clinical isolates were collected from 33 duodenal ulcer, 41 nonulcer related dyspepsia, 14 gastric ulcer, and 12 gastric malignancy patients. Polymerase chain reaction (PCR) assays were performed for cagA, cagC, cagE, cagF, and cagN in the cagI region, cagT and orf13 in the cagII region, and IS605 and iceA1 in all H. pylori isolates. Gastric histology of the infected host was reviewed using the updated Sydney system.
All strains were positive for all the selected genes in the PAI. PCR amplification found IS605 in 17%, while colony hybridization revealed it in 36% of strains. The prevalence of the cagA gene detected by PCR using cagA1, cagA2, and cagA3 primers was 26, 100, and 100%, respectively. The iceA1 gene existed in 72% of the H. pylori isolates. The mean ulcer size and the severity of acute gastric inflammation in patients infected with iceA1-positive strains were significantly greater than in those infected with iceA1-negative strains (p < 0.05).
All clinical H. pylori isolates from different gastric diseases in our Taiwanese patients were positive for the PAI, but only 36% of these isolates carried an IS605 insertion. The selected genes in the PAI were not correlated with disease outcome. The determination of cagA prevalence is based on the selection of suitable primers. In contrast, bacterial factors such as the presence of iceAl could be related to severity of gastric inflammation and increase in ulcer size in H. pylori-infected patients.
空泡毒素相关基因（cag）致病岛（PAI）的存在可能增强幽门螺杆菌的毒力。本研究旨在确定台湾地区幽门螺杆菌菌株中PAI、IS605和iceA1基因型的流行情况，以及这些基因型是否与临床疾病类型或胃部病理改变相关。
从33例十二指肠溃疡、41例非溃疡相关性消化不良、14例胃溃疡和12例胃癌患者中收集了100株临床分离株。对所有幽门螺杆菌分离株进行聚合酶链反应（PCR）检测，检测cagI区域的cagA、cagC、cagE、cagF和cagN，cagII区域的cagT和orf13，以及IS605和iceA1。采用更新后的悉尼系统对感染宿主的胃组织学进行评估。
所有菌株PAI中所选基因均为阳性。PCR扩增发现17%的菌株存在IS605，而菌落杂交显示36%的菌株存在该基因。使用cagA1、cagA2和cagA3引物通过PCR检测到的cagA基因流行率分别为26%、100%和100%。72%的幽门螺杆菌分离株存在iceA1基因。感染iceA1阳性菌株的患者的平均溃疡大小和急性胃炎症严重程度显著大于感染iceA1阴性菌株的患者（p<0.05）。
我们台湾地区患者中来自不同胃部疾病的所有临床幽门螺杆菌分离株PAI均为阳性，但这些分离株中只有36%携带IS605插入。PAI中所选基因与疾病结局无关。cagA流行率的测定取决于合适引物的选择。相比之下，诸如iceA1存在等细菌因素可能与幽门螺杆菌感染患者的胃炎症严重程度和溃疡大小增加有关。
