Levels of interleukin-18 are markedly increased in Helicobacter pylori-Infected gastric mucosa among patients with specific IL18 genotypes
Levels of interleukin-18 are markedly increased in Helicobacter pylori-Infected gastric mucosa among patients with specific IL18 genotypes
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DOI：
10.1086/588196
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发表时间：
2008-06-15
影响因子：
6.4
通讯作者：
Yamaoka, Yoshio
中科院分区：
文献类型：
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作者：
Sakai, Kyoko;Kita, Masakazu;Yamaoka, Yoshio
背景资料。幽门螺杆菌感染胃粘膜的细胞免疫应答主要是辅助性T细胞1型。采用逆转录-聚合酶链式反应(RT-PCR)和酶联免疫吸附试验检测胃粘膜活检组织中IL-18、IL-12和干扰素(IFN)-γ水平，并用聚合酶链式反应(PCR)检测IL-18基因多态性。对128例患者(非溃疡性消化不良56例，胃溃疡28例，十二指肠溃疡28例，胃癌16例)的活检标本进行了检测，其中96例有幽门螺杆菌感染。IL-18水平在幽门螺杆菌感染的粘膜中显著上调(P<；.001)，而IL-12和干扰素-γ水平与幽门螺杆菌状态无关。IL-18水平与干扰素-γ水平仅在感染患者呈正相关(R=0.31~0.51)。IL-18水平是幽门螺杆菌感染黏膜单核细胞浸润的决定因素(P=.001)。携带IL18-607C/C和-137G/G基因的幽门螺杆菌感染者的IL-18水平高于其他基因携带者，且治疗失败的可能性较大。幽门螺杆菌感染可诱导胃粘膜产生IL-18。幽门螺杆菌感染患者IL18-607C/C和-137G/G的患者IL-18水平较高，从而导致严重的胃炎症。IL18基因可能是预测根除治疗效果的一个指标。
Background. The cellular immune response in gastric mucosa infected with Helicobacter pylori is proposed to be predominantly of the T helper cell type 1 type.Methods. Interleukin (IL)-18, IL-12, and interferon (IFN)-gamma levels were measured in gastric mucosal biopsy specimens by reverse-transcription polymerase chain reaction (PCR) and by enzyme-linked immunosorbent assay; IL18 polymorphisms were determined by PCR.Results. Biopsy specimens from 128 patients (56 with nonulcer dyspepsia, 28 with gastric ulcers, 28 with duodenal ulcers, and 16 with gastric cancer) were examined; 96 patients had H. pylori infection. IL-18 levels were markedly up-regulated in mucosa infected with H. pylori (P < .001), whereas IL-12 and IFN-gamma levels were independent of H. pylori status. IL-18 levels correlated with IFN-gamma levels only in infected patients (R = 0.31 to R = 0.51). IL-18 levels were the determining factor for monocyte infiltration in H. pylori-infected mucosa (P = .001). H. pylori-infected patients displaying IL18-607C/C and-137G/G had higher IL-18 levels than did those with other genotypes and were more likely to experience treatment failure.Conclusion. H. pylori infection induces IL-18 in the gastric mucosa. H. pylori-infected patients with IL18-607C/C and -137G/G have higher IL-18 levels, which causes severe gastric inflammation. IL18 genotype might be a marker for predicting the effects of eradication therapy.