首页> 美国卫生研究院文献>Mediators of Inflammation >Serum levels of tumor necrosis factor-alpha interleukin-6 and interleukin-8 are not increased in dyspeptic patients with Helicobacter pylori-associated gastritis.
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Serum levels of tumor necrosis factor-alpha interleukin-6 and interleukin-8 are not increased in dyspeptic patients with Helicobacter pylori-associated gastritis.

机译:在消化不良的幽门螺杆菌相关性胃炎患者中肿瘤坏死因子-α白介素-6和白介素-8的血清水平没有增加。

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摘要

INTRODUCTION: Helicobacter pylori (H. pylori) is a non-invasive microorganism causing intense gastric mucosal inflammatory and immune reaction. H. pylori-induced gastric mucosal cytokine overproduction has been clearly documented previously. The stomach has a large surface area and continuous spill-over of locally produced cytokines into the blood stream is a possibility. There are few and conflicting data on circulatory proinflammatory cytokine levels in patients with H. pylori infection. MATERIALS AND METHODS: Forty-two dyspeptic patients were enrolled into the study. The presence of H. pylori infection was diagnosed with antral histopathologic examination. After overnight fasting; serum samples were obtained from each patient to determine circulating interleukin (IL)-6, IL-8 and tumor necrosis factor-alpha (TNF-alpha) levels. RESULTS: H. pylori was shown in 30 cases using Giemsa stain in antral histopathologic evaluation. Twelve cases were negative for H. pylori staining. Both the age and sex distribution had an insignificant difference in both H pylori-positive and H. pylori-negative groups. The mean circulatory levels of IL-6, IL-8 and TNF-a in both groups were not different. The situation was same in respect to the serum levels of these cytokines and the degree of inflammation, H. pylori density and activation scores according to Sydney classification. CONCLUSION: We could not show elevated circulatory levels of IL-6, IL-8 and TNF-alpha in H. pylori-infected cases. We believe that H. pylori-related cytokine activation become concentrated on gastric mucosa and this pathogen-induced local inflammatory cascade does not cause changes in circulatory levels of these cytokines. Moreover, there is no correlation between the levels of serum cytokines and Sydney parameters.
机译:简介:幽门螺杆菌(H. pylori)是一种非侵入性微生物,可引起强烈的胃粘膜炎性反应和免疫反应。幽门螺杆菌诱导的胃粘膜细胞因子的过度生产先前已被明确记录。胃的表面积很大,有可能将局部产生的细胞因子连续溢出到血液中。幽门螺杆菌感染患者循环中促炎细胞因子水平的数据很少且相互矛盾。材料与方法:42名消化不良的患者被纳入研究。通过肛门组织病理学检查诊断为幽门螺杆菌感染。过夜禁食后;从每位患者获得血清样本,以确定循环白介素(IL)-6,IL-8和肿瘤坏死因子-α(TNF-α)水平。结果:30例经Giemsa染色显示的幽门螺杆菌在肛门组织病理学评估中显示。十二例幽门螺杆菌染色阴性。幽门螺杆菌阳性和幽门螺杆菌阴性组的年龄和性别分布均无显着差异。两组中IL-6,IL-8和TNF-α的平均循环水平无差异。关于这些细胞因子的血清水平以及根据悉尼分类的炎症程度,幽门螺杆菌密度和激活评分,情况相同。结论:在幽门螺杆菌感染的病例中,我们无法显示IL-6,IL-8和TNF-α的循环水平升高。我们相信幽门螺杆菌相关的细胞因子激活变得集中在胃粘膜上,这种病原体诱导的局部炎症级联反应不会引起这些细胞因子的循环水平改变。此外,血清细胞因子水平和悉尼参数之间没有相关性。

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