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首页> 外文期刊>Infection and immunity >Evaluation of the Association of Nine Helicobacter pylori Virulence Factors with Strains Involved in Low-Grade Gastric Mucosa-Associated Lymphoid Tissue Lymphoma
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Evaluation of the Association of Nine Helicobacter pylori Virulence Factors with Strains Involved in Low-Grade Gastric Mucosa-Associated Lymphoid Tissue Lymphoma

机译：九株幽门螺杆菌毒力因子与低级胃黏膜相关淋巴组织淋巴瘤相关菌株的关系评估

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Helicobacter pylori has been associated with the development of two malignant diseases: gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Although the cag pathogenicity island, especially the cagA gene, has been linked with adenocarcinoma, few data concerning H. pylori pathogenic factors involved in low-grade gastric MALT lymphoma are available. The goal of this study was to analyze the prevalence of and correlation between genes coding for seven H. pylori virulence factors (cagA, cagE, vacA, iceA, babA, hopQ, and oipA) and two novel adhesins (sabA and hopZ) by comparing a collection of 43 H. pylori strains isolated from patients with low-grade gastric MALT lymphoma to 39 strains isolated from age-matched patients with gastritis only. Our results show that taken individually, none of the nine genes tested can be considered associated with MALT strains and allow us to conclude that MALT pathogenesis is not linked with more proinflammatory H. pylori strains. We demonstrated that in patients infected with strains harboring the iceA1 allele, sabA functional status, and hopZ “off” status, the odds of developing a MALT lymphoma were 10 times higher. However, the low prevalence of such strains (10 of 43 MALT strains) renders this triple association a low-sensitivity marker for MALT strains. Our data confirmed that H. pylori virulence factors are correlated with one another. If the involvement of H. pylori in MALT lymphoma is well established, the pathomechanism by which gastric lymphoma occurs remains to be identified.
机译：幽门螺杆菌与两种恶性疾病的发展有关：胃腺癌和胃黏膜相关淋巴样组织（MALT）淋巴瘤。尽管 cag 致病岛，特别是 cagA 基因已经与腺癌相关，但很少有关于 H的数据。目前已有低级胃MALT淋巴瘤的幽门螺杆菌致病因素。这项研究的目的是分析编码7个 H的基因的普遍性和相关性。幽门螺杆菌毒力因子（ cagA ， cagE ， vacA ， iceA ， babA ， hopQ 和 oipA ）和两个新型粘附素（ sabA 和 hopZ ），方法是比较43 H。从低级胃MALT淋巴瘤患者中分离出pylori 菌株，从年龄匹配的胃炎患者中分离出39株菌株。我们的结果表明，单独进行测试，不能将9个基因中的任何一个与MALT菌株相关联，并且可以使我们得出结论，MALT的发病机理与更多的促炎性 H不相关。幽门螺杆菌菌株。我们证明了在感染带有 iceA1 等位基因， sabA 功能状态和 hopZ “关闭”状态的菌株的患者中，发生MALT淋巴瘤高出10倍。然而，这种菌株的低流行（43个MALT菌株中的10个）使得该三联体成为MALT菌株的低敏感性标记。我们的数据证实了 H。幽门螺杆菌毒力因子彼此相关。如果 H参与。 MALT淋巴瘤中的幽门螺杆菌已经很成熟，胃淋巴瘤的发病机制尚待确定。

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