Interaction of Helicobacter pylori-induced follicular gastritis and autoimmune gastritis in BALB/c mice with post-thymectomy autoimmune gastritis

被引:14
|
作者
Okazaki, K [1 ]
Ohana, M
Oshima, C
Uchida, K
Nishi, T
Iwano, M
Fukui, T
Kawasaki, K
Matsuura, M
Asada, M
Tamaki, H
Hiai, H
Chiba, T
机构
[1] Kyoto Univ Hosp, Dept Endoscop Med & Gastroenterol, Kyoto 606, Japan
[2] Kansai Med Univ, Dept Internal Med 3, Moriguchi, Osaka 5708507, Japan
[3] Kyoto Univ, Grad Sch Med, Dept Pathol & Biol Dis, Kyoto, Japan
关键词
autoimmune gastritis; Helicobacter pylori; Th1/2 immune balance;
D O I
10.1007/s00535-003-1219-3
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background. There is still controversy about the relationship between Helicobacter pylori infection and autoimmune gastritis. The aim of this study was to clarify whether or not H. pylori infection interacts with the development of autoimmune gastritis. Methods. Neonatally thymectomized BALB/c mice with autoimmune gastritis received orally administered H. pylori and were examined histologically and serologically. The T-helper (Th)1/Th2 immune balance in the microenvironment of the stomach was evaluated by reverse-transcriptase-polymerase chain reaction (RT-PCR) for interferon (IFN)-gamma and interleukin (IL)-4. Results. Uninfected mice showed disappearance of parietal cells, and upregulation of IFN-gamma, but no germinal center formation. The infected neonatally thymectomized mice showed follicular gastritis, preserved parietal cells, decreased serum anti-parietal antibodies, and upregulation of IL-4 and IFN-gamma. Conclusions. H. pylori infection changes the microenvironment of the gastric mucosa by inducing a Th2 immune response in addition to a Th1 response, and regresses autoimmune gastritis in neonatally thymectomized BALB/c mice.
引用
收藏
页码:1131 / 1137
页数:7
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