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幽门螺杆菌胃炎中抗胃自身抗体的黏膜产生

Mucosal production of antigastric autoantibodies in Helicobacter pylori gastritis.

作者信息

Faller G, Ruff S, Reiche N, Hochberger J, Hahn E G, Kirchner T

机构信息

Institute of Pathology and Department of Internal Medicine I, University of Erlangen-Nuremberg, Germany.

出版信息

Helicobacter. 2000 Sep;5(3):129-34. doi: 10.1046/j.1523-5378.2000.00020.x.

DOI:10.1046/j.1523-5378.2000.00020.x
PMID:10971676
Abstract

BACKGROUND

Apart form bacterial virulence factors of Helicobacter pylori, certain host factors influence the pathogenesis of H. pylori gastritis. In particular, antigastric autoantibodies that are detectable in the sera of a substantial proportion of H. pylori were shown to correlate with the development of gastric atrophy. The aim of this study was to analyze the possible antigastric autoimmune response in H. pylori gastritis at the site where the action is, i.e. , in the gastric mucosa.

MATERIAL AND METHODS

Gastric biopsy specimens from antrum and corpus mucosa of 24 H. pylori-infected and of 33 noninfected patients were cultured for 3 days, and tissue culture supernatants were analyzed for the amount of locally produced IgA and IgG. Antigastric autoantibodies were screened in the sera and in the supernatants by means of immunohistochemistry.

RESULTS

The infected patients had significantly higher concentrations of locally produced IgA, whereas the IgG concentrations were virtually the same in infected and noninfected patients. IgG or IgA antigastric autoantibodies, or both, were detectable only in the sera (38%) and supernatants (17%) of infected patients. Interestingly, the patient with the strongest local autoimmune response showed body-predominant H. pylori gastritis, with destruction of gastric glands and atrophy of the body mucosa.

CONCLUSIONS

These results demonstrate that antigastric autoimmune reactions are detectable at the site of the disease and might be relevant for the pathogenesis of gastric mucosa atrophy in H. pylori gastritis.

摘要

背景

除幽门螺杆菌的细菌毒力因子外,某些宿主因素也会影响幽门螺杆菌胃炎的发病机制。特别是,在相当一部分幽门螺杆菌感染者血清中可检测到的抗胃自身抗体与胃萎缩的发生有关。本研究的目的是分析幽门螺杆菌胃炎发病部位(即胃黏膜)可能存在的抗胃自身免疫反应。

材料与方法

对24例幽门螺杆菌感染患者和33例未感染患者的胃窦和胃体黏膜活检标本进行3天培养,并分析组织培养上清液中局部产生的IgA和IgG量。通过免疫组织化学方法在血清和上清液中筛选抗胃自身抗体。

结果

感染患者局部产生的IgA浓度显著更高,而感染患者和未感染患者的IgG浓度基本相同。仅在感染患者的血清(38%)和上清液(17%)中可检测到IgG或IgA抗胃自身抗体,或两者均有。有趣的是,局部自身免疫反应最强的患者表现为胃体为主的幽门螺杆菌胃炎,伴有胃腺破坏和胃体黏膜萎缩。

结论

这些结果表明,在疾病部位可检测到抗胃自身免疫反应,这可能与幽门螺杆菌胃炎胃黏膜萎缩的发病机制有关。

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Mucosal production of antigastric autoantibodies in Helicobacter pylori gastritis.幽门螺杆菌胃炎中抗胃自身抗体的黏膜产生
Helicobacter. 2000 Sep;5(3):129-34. doi: 10.1046/j.1523-5378.2000.00020.x.
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Antigastric autoantibodies in Helicobacter pylori infection: implications of histological and clinical parameters of gastritis.幽门螺杆菌感染中的抗胃自身抗体:胃炎组织学和临床参数的意义
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[Helicobacter pylori and antigastric autoimmunity].[幽门螺杆菌与抗胃自身免疫]
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The gastric H+,K+-ATPase is a major autoantigen in chronic Helicobacter pylori gastritis with body mucosa atrophy.胃H⁺,K⁺-ATP酶是慢性幽门螺杆菌性胃体黏膜萎缩性胃炎中的一种主要自身抗原。
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Apoptosis in chronic gastritis and its correlation with antigastric autoantibodies.慢性胃炎中的细胞凋亡及其与抗胃自身抗体的相关性。
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Evidence of novel pathogenic pathways for the formation of antigastric autoantibodies in Helicobacter pylori gastritis.幽门螺杆菌胃炎中抗胃自身抗体形成的新致病途径的证据。
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Role of antigastric autoantibodies in chronic Helicobacter pylori infection.抗胃自身抗体在幽门螺杆菌慢性感染中的作用。
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