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International Immunology Advance Access originally published online on February 20, 2007
International Immunology 2007 19(4):435-446; doi:10.1093/intimm/dxm008
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Essential role of Peyer's patches in the development of Helicobacter-induced gastritis

Keiichi Kiriya, Norihiko Watanabe, Akiyoshi Nishio, Kazuichi Okazaki1, Masahiro Kido, Kazuyuki Saga, Junya Tanaka, Takuji Akamatsu, Shinya Ohashi, Masanori Asada, Toshiro Fukui and Tsutomu Chiba

Department of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan
1 Present address: Department of Gastroenterology and Hepatology, Kansai Medical University, 2-3-1 Shinmachi, Hirakata, Osaka 573-1191, Japan

Correspondence to: T. Chiba; E-mail: chiba{at}kuhp.kyoto-u.ac.jp

Helicobacter bacteria colonize in the stomach and induce strong, specific local and systemic humoral and cell-mediated immunity. Helicobacter binds to the host epithelial cells, directly triggering the recruitment of neutrophils. Local inflammatory processes in the gastric mucosa are followed by extensive immune cell infiltration, resulting in chronic active gastritis characterized by a marked infiltration of Th1 cytokine-producing CD4+ T cells. The mechanisms underlying the development of Th1 cell-mediated chronic gastritis, however, are not clear. Peyer's patches (PPs), the major inductive sites for mucosal immunity in the gut system, might orchestrate Helicobacter-specific local and systemic humoral and cell-mediated immunity. To examine the roles of PPs in the development of Helicobacter-induced gastritis, we generated PP-null mice that normally develop well-organized lymphoid organs except for PPs and intra-gastrically infected the resulting PP-null mice with Helicobacter felis. PP deficiency severely impaired both the development of Th1 cell-mediated gastritis induced by Helicobacter and the production of anti-Helicobacter antibodies despite marked bacterial colonization of the gastric mucosa. Although PP deficiency did not impair the differentiation of Helicobacter-specific CD4+ T cells into IFN-{gamma}—producing Th1 cells, Helicobacter-specific IFN-{gamma}—producing CD4+ T cells in PP-null mice lacked the ability to migrate into Helicobacter-colonized gastric mucosa. These findings suggest that PPs have an important role in Helicobacter-specific local and systemic humoral and cell-mediated immunity, including the development of Helicobacter-induced gastritis.

Keywords: CCR9 CD4+ T cells, IFN-{gamma}, production, migration, Peyer's patch-null mice

Transmitting editor: M. Miyasaka

Received 17 June 2006, accepted 18 January 2007.


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[Abstract] [Full Text] [PDF]


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