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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Host Cell Responses to Genotypically Similar Helicobacter pylori Isolates from United States and Japan
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Host Cell Responses to Genotypically Similar Helicobacter pylori Isolates from United States and Japan

机译：宿主细胞对来自美国和日本的基因型相似的幽门螺杆菌分离株的反应

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Associations of Helicobacter pylori genotypes with disease differ between Western countries and Asia. Therefore, we directly compared histopathological and in vitro responses to clinical isolates with similar genotypes. Sixty-three cagA+ vacAs1/m1 H. pylori isolates (United States, n = 24; Japan, n = 39) and eight cagA-negative vacAs2/m2 strains were incubated with AGS cells, and supernatants were assayed for interleukin-8 (IL-8) and for DNA fragmentation. CagA tyrosine phosphorylation in AGS cells and the sequence of the putative HP0638 (oipA) signal sequence region were determined for 22 representative strains. HP0638 and/or cag island mutant strains were created and examined in IL-8 and CagA tyrosine phosphorylation assays. Levels of IL-8 induction and DNA fragmentation were similar in the U.S. and Japanese cagA+ vacAs1/m1 isolates. All 10 of the isolates with the highest IL-8 induction and 8 of the 10 isolates with the lowest IL-8 induction had an in-frame oipA open reading frame, and all 10 of the isolates with the highest IL-8 induction and 7 of the 10 isolates with the lowest IL-8 induction induced CagA tyrosine phosphorylation in AGS cells. Eight isolates from gastric ulcer patients induced significantly more apoptosis in vitro, and more severe gastritis and atrophy in vivo, than other Japanese isolates. Disruption of HP0638 did not affect IL-8 induction or CagA tyrosine phosphorylation. Thus, H. pylori cagA+ vacAs1/m1 isolates from the United States and Japan induce similar IL-8 and apoptosis levels. Inactivation of HP0638 does not alter epithelial responses mediated by the cag island in vitro. Assessment of apoptosis in vitro identified a group of H. pylori isolates that induce more severe gastric inflammation and atrophy.
机译：在西方国家和亚洲，幽门螺杆菌基因型与疾病的相关性有所不同。因此，我们直接比较了对具有相似基因型的临床分离株的组织病理学和体外反应。 cagA + vacA s1 / m1 H六十三。幽门螺杆菌分离株（美国， n = 24;日本， n = 39）和8个 cagA 阴性的 vacA s2 / m2菌株与AGS细胞孵育，并分析上清液中的白介素8（IL-8）和DNA片段。确定了22个代表性菌株在AGS细胞中的CagA酪氨酸磷酸化和假定的HP0638（ oipA ）信号序列区域的序列。 HP0638和/或 cag 岛突变株被创建并在IL-8和CagA酪氨酸磷酸化测定中进行了检查。在美国和日本的 cagA + vacA s1 / m1分离株中，IL-8诱导水平和DNA片段水平相似。 IL-8诱导率最高的所有10个分离株和IL-8诱导率最低的10个分离株中的8个具有框内 oipA 开放阅读框，而所有10个具有IL-8诱导的分离株。在AGS细胞中，IL-8诱导率最高，而IL-8诱导率最低的10个分离株中有7个诱导CagA酪氨酸磷酸化。与其他日本分离株相比，来自胃溃疡患者的八种分离株在体外诱导的细胞凋亡明显更多，在体内诱导出更严重的胃炎和萎缩。 HP0638的破坏不影响IL-8诱导或CagA酪氨酸磷酸化。因此， H。来自美国和日本的幽门螺杆菌cagA + vacA s1 / m1分离株诱导相似的IL-8和细胞凋亡水平。 HP0638的失活不会改变 cag 岛在体外介导的上皮反应。体外凋亡评估鉴定出一组 H。幽门螺杆菌分离株，引起更严重的胃部炎症和萎缩。

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