The cag pathogenicity island of Helicobacter pylori is disrupted in the majority of patient isolates from different human populations
The cag pathogenicity island of Helicobacter pylori is disrupted in the majority of patient isolates from different human populations
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DOI：
10.1128/jcm.42.11.5302-5308.2004
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发表时间：
2004-11-01
影响因子：
9.4
通讯作者：
Ahmed, N
中科院分区：
文献类型：
--
作者：
Kauser, F;Khan, AA;Ahmed, N
cag致病岛（cag-PAI）是幽门螺杆菌的主要毒力决定因子之一。推测该岛的染色体完整性或缺失在H.幽门。我们通过使用特异性侧翼和内部锚定的PCR引物来确定cag-PAI的完整性，以了解携带具有体内促炎行为的完全完整的cag-PAI的菌株的地理分布。从8个不同的地理区域获得的335个菌株的基因型进行了研究的基础上选择的8个位点。cag-PAI似乎在世界各地的大多数患者分离株中被破坏。日本分离株cag-PAI保守性最高（57.1%）。然而，只有18.6%的秘鲁和12%的印度分离株携带完整的cag-PAI。cag-PAI在欧洲和非洲菌株的完整性是最小的。来自哥斯达黎加的所有10个菌株都有重排。总体而言，与其他血统的菌株相比，东亚血统的大多数菌株被发现具有完整的cag-PAI。我们还发现cagE和cagT基因重排的频率（18%）低于cagA基因（27%）。我们试图将cag-PAI重排模式与疾病结局联系起来。cagA，cagE和cagT基因的缺失频率在良性病例中高于严重溃疡和胃癌的分离株。相反，cagA启动子和cag-PAI的左端经常重排或删除分离株与严重的病理。分析cag-PAI基因型与不同的气候历史将有助于我们了解病原体-宿主相互作用的健康和疾病。
The cag pathogenicity island (cag-PAI) is one of the major virulence determinants of Helicobacter pylori. The chromosomal integrity of this island or the lack thereof is speculated to play an important role in the progress of the gastroduodenal pathology caused by H. pylori. We determined the integrity of the cag-PAI by using specific flanking and internally anchored PCR primers to know the biogeographical distribution of strains carrying fully integral cag-PAI with proinflammatory behavior in vivo. Genotypes based on eight selected loci were studied in 335 isolates obtained from eight different geographic regions. The cag-PAI appeared to be disrupted in the majority of patient isolates throughout the world. Conservation of cag-PAI was highest in Japanese isolates (57.1%). However, only 18.6% of the Peruvian and 12% of the Indian isolates carried an intact cag-PAI. The integrity of cag-PAI in European and African strains was minimal. All 10 strains from Costa Rica had rearrangements. Overall, a majority of the strains of East Asian ancestry were found to have intact cag-PAI compared to strains of other descent. We also found that the cagE and cagT genes were less often rearranged (18%) than the cagA gene (27%). We attempted to relate cag-PAI rearrangement patterns to disease outcome. Deletion frequencies of cagA, cagE, and cagT genes were higher in benign cases than in isolates from severe ulcers and gastric cancer. Conversely, the cagA promoter and the left end of the cag-PAI were frequently rearranged or deleted in isolates linked to severe pathology. Analysis of the cag-PAI genotypes with a different biogeoclimatic history will contribute to our understanding of the pathogen-host interaction in health and disease.