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首页> 外文期刊>Infection and immunity >Role of Helicobacter pylori cag Region Genes in Colonization and Gastritis in Two Animal Models
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Role of Helicobacter pylori cag Region Genes in Colonization and Gastritis in Two Animal Models

机译：幽门螺杆菌cag区域基因在两种动物模型中的定殖和胃炎中的作用

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The Helicobacter pylori chromosomal region known as the cytotoxin-gene associated pathogenicity island (cag PAI) is associated with severe disease and encodes proteins that are believed to induce interleukin (IL-8) secretion by cultured epithelial cells. The objective of this study was to evaluate the relationship between the cag PAI, induction of IL-8, and induction of neutrophilic gastric inflammation. Germ-free neonatal piglets and conventional C57BL/6 mice were given wild-type or cagdeficient mutant derivatives of H. pylori strain 26695 or SS1. Bacterial colonization was determined by plate count, gastritis and neutrophilic inflammation were quantified, and IL-8 induction in AGS cells was determined by enzyme-linked immunosorbent assay. Deletion of the entire cag region or interruption of thevirB10 or virB11 homolog had no effect on bacterial colonization, gastritis, or neutrophilic inflammation. In contrast, these mutations had variable effects on IL-8 induction, depending on the H. pylori strain. In the piglet-adapated strain 26695, which induced IL-8 secretion by AGS cells, deletion of the cag PAI decreased induction. In the mouse-adapted strain SS1, which did not induce IL-8 secretion, deletion of thecagII region or interruption of any of threecag region genes increased IL-8 induction. These results indicate that in mice and piglets (i) neither the cag PAI nor the ability to induce IL-8 in vitro is essential for colonization or neutrophilic inflammation and (ii) there is no direct relationship between the presence of the cag PAI, IL-8 induction, and neutrophilic gastritis.
机译：幽门螺杆菌（Helicobacter pylori）染色体区域，称为细胞毒素基因相关致病岛（ cag PAI），与严重疾病相关，并编码被认为诱导白介素（IL-8）的蛋白质）由培养的上皮细胞分泌。这项研究的目的是评估 cag PAI，IL-8的诱导和嗜中性胃炎的诱导之间的关系。给无胚新生仔猪和常规C57BL / 6小鼠施用野生型或 cag 缺陷的 H突变体。幽门螺杆菌26695或SS1。通过板计数确定细菌定植，定量胃炎和嗜中性粒细胞炎症，并且通过酶联免疫吸附测定确定在AGS细胞中的IL-8诱导。删除整个 区域或中断 virB10 或 virB11 同系物对细菌定植，胃炎或嗜中性炎症没有影响。相反，取决于 H，这些突变对IL-8诱导具有可变的影响。幽门螺杆菌在适应小猪的26695株诱导AGS细胞分泌IL-8的过程中， cag PAI的缺失降低了诱导。在不诱导IL-8分泌的适应小鼠的SS1株中， cag II区的缺失或三个 cag 区基因中任一个的中断都会增加IL-8。感应。这些结果表明，在小鼠和仔猪中，（i） cag PAI或体外诱导IL-8的能力对于定植或嗜中性粒细胞炎症都不是必需的，并且（ii）两者之间没有直接关系。 cag PAI，IL-8诱导和嗜中性胃炎的存在。

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