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Infection and Immunity, January 2000, p. 100-106, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Induction of Follicular Gastritis following Postthymectomy Autoimmune Gastritis in Helicobacter pylori-Infected BALB/c Mice

Chikashi Oshima,1,2,3 Kazuichi Okazaki,2,3,* Yumi Matsushima,2,3 Mitsutaka Sawada,3 Tsutomu Chiba,2,3 Kiyoyuki Takahashi,4 Hiroshi Hiai,5 Tomoya Katakai,6 Shinpei Kasakura,7 and Tohru Masuda1

Department of Immunology,1 Department of Endoscopic Medicine,2 Department of Gastroenterology,3 and Department of Pathology,5 Faculty of Medicine, College of Medical Technology,4 and Center for Molecular Biology and Genetics,6 Graduate School of Medicine, Kyoto University, Kyoto, and Kobe City General Hospital, Kobe,7 Japan

Received 6 July 1999/Returned for modification 23 August 1999/Accepted 5 October 1999

Helicobacter pylori is the major causative agent of chronic antral gastritis and is thought to be involved in the pathogenesis of mucosa-associated lymphoid tissue lymphoma (MALToma) developing in the human stomach. The aim of this study was to clarify whether corporal autoimmune gastritis (AIG), which is known to decrease acidity due to destruction of parietal cells, predisposes mice to H. pylori infection, thereby leading to MALToma-like pathology. BALB/c mice in which AIG had been induced by thymectomy 3 days after birth (AIG mice) were used. The AIG mice were orally administered mouse-adapted H. pylori at the age of 6 weeks and were examined histologically and serologically after 2 to 12 months. The results were compared with those obtained from uninfected AIG mice and infected normal mice. Germinal centers were induced in the corpus in 57% of the H. pylori-infected AIG mice, which elicited anti-H. pylori antibody responses in association with upregulation of interleukin-4 (IL-4) mRNA. In these mice, parietal cells remained in the corpus mucosa. These findings were in contrast to those with the uninfected AIG mice: fundic gland atrophy due to disappearance of parietal cells associated with upregulation of gamma interferon, but not IL-4, mRNA and no germinal center formation in the corpus. These observations suggest that AIG alters the infectivity of H. pylori, leading to MALToma-like follicular gastritis, at an early stage after H. pylori infection.

* Corresponding author. Mailing address: Department of Endoscopic Medicine and Gastroenterology, Faculty of Medicine, Kyoto University, Shogoin-Kawaharamachi, Sakyo 606, Kyoto, Japan. Phone: 81-75-751-3413. Fax: 81-75-751-3414. E-mail: okak{at}kuhp.kyoto-u.ac.jp.

Infection and Immunity, January 2000, p. 100-106, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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