Helicobacter pylori with the Intact dupA Cluster is more Virulent than the Strains with the Incomplete dupA Cluster

Helicobacter pylori with the Intact dupA Cluster is more Virulent than the Strains with the Incomplete dupA Cluster
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具有完整 dupA 簇的幽门螺杆菌比具有不完整 dupA 簇的菌株毒性更强

DOI:
10.1007/s00284-015-0812-z
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发表时间:
2015-04
影响因子:
2.6
通讯作者:
Shao, Shi-he
Shao, Shi-he
中科院分区:
生物学4区
文献类型:
--
作者:
Hao, Jun-ling;Wu, Chun-mei;Gao, Xiao-zhong;Shao, Shi-he

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十二指肠溃疡促进基因(dupA)位于幽门螺杆菌(h.p ylori)的可塑性区,预计与dupA周围的vir基因形成IV型分泌系统(T4SS)。在这项研究中,我们调查了东北沿海地区dupA集群状态与幽门螺杆菌毒力的关系。对262株慢性胃炎幽门螺杆菌进行PCR和Western blot检测,检测其dupA聚类状态、cag PAI基因和vacA基因型。对活检标本进行组织病理学评估,以分析dupA簇与炎症反应之间的关系。分别测定胃黏膜和与幽门螺杆菌共培养的GES-1细胞的IL-8产量,分析dupA簇状态与IL-8产量的关系。我们发现,dupA阳性幽门螺杆菌患者胃粘膜炎症细胞浸润明显高于dupA阴性菌株患者(1.73±0.60,p < 0.01),包括完全dupA簇幽门螺杆菌(2.71±0.79)和不完全dupA簇幽门螺杆菌(2.09±0.61),而根据dupA簇的状态,胃粘膜萎缩无显著差异。完全dupA组胃粘膜IL-8水平高于其他组(p < 0.01),完全dupA组GES-1细胞的IL-8产量(1527.9±180.0 pg/ml)也显著高于不完全dupA组(1229.4±75.3 pg/ml, p < 0.01)或dupA阴性组(1201.9±92.3 pg/ml, p < 0.01)。综上所述,幽门螺杆菌中完全dupA簇与炎症细胞浸润和IL-8分泌有关,具有完全dupA簇的幽门螺杆菌菌株似乎比具有不完全dupA簇或dupA阴性的其他菌株毒性更强。
The duodenal ulcer promoting gene (dupA), located in the plasticity region of Helicobacter pylori (H. pylori), is predicted to form a type IV secretory system (T4SS) with vir genes around dupA. In the study, we investigated the association between the dupA cluster status and the virulence of H. pylori in a littoral region of Northeast China. Two hundred and sixty-two H. pylori strains isolated from the chronic gastritis were examined to evaluate the dupA cluster status, cag PAI genes and vacA genotype using PCR and Western blot. Histopathologic evaluations of biopsy specimens were performed to analysis the association between the dupA cluster and the inflammatory response. IL-8 productions in gastric mucosa and from GES-1 cells co-cultured with H. pylori were measured, respectively, to analysis the association between the dupA cluster status and IL-8 production. We found that gastric mucosal inflammatory cell infiltration was significantly higher in patients with dupA-positive H. pylori, including H. pylori with complete dupA cluster (2.71 ± 0.79) and incomplete dupA cluster (2.09 ± 0.61) than in patients with dupA-negative strain (1.73 ± 0.60, p < 0.01), whereas no significant difference in the gastric mucosal atrophy was found according to the status of dupA cluster. Gastric mucosal IL-8 levels were higher in the complete dupA cluster group than in other groups (p < 0.01), and IL-8 production from GES-1 cells was also significantly higher in strains with a complete dupA cluster (1527.9 ± 180.0 pg/ml) than in those with an incomplete dupA cluster (1229.4 ± 75.3 pg/ml, p < 0.01) or those with dupA negative (1201.9 ± 92.3 pg/ml, p < 0.01). In conclusion, the complete dupA cluster in H. pylori is associated with inflammatory cell infiltration and IL-8 secretion, and H. pylori strain with a complete dupA cluster seems to be more virulent than other strains with the incomplete dupA cluster or dupA negative.
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