Enhancement of adherence of Helicobacter pylori to host cells by virus: possible mechanism of development of symptoms of gastric disease

Enhancement of adherence of Helicobacter pylori to host cells by virus: possible mechanism of development of symptoms of gastric disease
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病毒增强幽门螺杆菌对宿主细胞的粘附:胃病症状发展的可能机制

DOI:
10.1007/s00795-017-0153-z
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发表时间:
2017
影响因子:
1.8
通讯作者:
Sano Kouichi
Sano Kouichi
中科院分区:
医学4区
文献类型:
--
作者:
Wu Hong;Nakano Takashi;Suzuki Youichi;Ooi Yukimasa;Sano Kouichi

文献摘要

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目前尚不清楚为什么并非所有幽门螺杆菌感染病例都会发生胃病。在这项研究中,我们分析了猿猴病毒5(SV 5)是否增强了H的粘附。幽门腺上皮细胞(AGS); pyloriin AGS(含SV 5)和SV 5感染的Vero细胞对H.光镜、扫描电镜和透射电镜观察pylorimixed与SV 5的关系。H.用抗-SV 5抗体处理的Vero细胞。扫描电镜和透射电镜观察显示,pylori粘附于AGS细胞表面,靠近SV 5颗粒。H. pyloritoSV 5感染Vero细胞后,细胞凋亡率明显高于对照组。相反,H. pylorito Vero细胞通过用抗SV 5抗体处理而减少。H.用扫描电镜和透射电镜观察pylorimixed与SV 5的结合情况。当在混合前用抗SV 5抗体处理SV 5时,未发生凝集。这些结果表明SV 5增强了H. pylorito宿主细胞,表明持续感染的病毒可能是增强H.幽门螺杆菌在人类中。
It remains unclear why gastric disease does not develop in all cases ofHelicobacter pyloriinfection. In this study, we analyzed whethersimian virus 5(SV5) enhanced adherence ofH. pylorito adenocarcinoma epithelial cells (AGS).H. pyloriin AGS (harboring SV5) and SV5-infected Vero cells, and an agglutination ofH. pylorimixed with SV5 were observed by light microscopy, scanning and transmission electron microscopies. The adherent rate ofH. pylorito SV5-infected Vero cells and treated with an anti-SV5 antibody was determined.H. pyloriadhered to the surface of AGS cells near SV5 particles, as shown by scanning and transmission electron microscopies. The adherence ofH. pylorito SV5-infected Vero cells was significantly enhanced compared with that to Vero cells. In contrast, the adherence ofH. pylorito Vero cells was decreased by treatment with the anti-SV5 antibody. Agglutination ofH. pylorimixed with SV5 was observed by scanning and transmission electron microscopies. Agglutination did not occur when SV5 was treated with the anti-SV5 antibody before mixing. These findings demonstrated that SV5 enhanced the adherence ofH. pylorito host cells, suggesting that a persistently infected virus may be a factor enhancing the pathogenicity ofH. pyloriin humans.