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Infection and Immunity, April 2003, p. 2153-2162, Vol. 71, No. 4
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.4.2153-2162.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Involvement of Myeloid Dendritic Cells in the Development of Gastric Secondary Lymphoid Follicles in Helicobacter pylori-Infected Neonatally Thymectomized BALB/c Mice
Toshiki Nishi,1 Kazuichi Okazaki,1* Kimio Kawasaki,1 Toshiro Fukui,1 Hiroyuki Tamaki,1 Minoru Matsuura,1 Masanori Asada,1 Tomohiro Watanabe,1 Kazushige Uchida,1 Norihiko Watanabe,1 Hiroshi Nakase,1 Masaya Ohana,1 Hiroshi Hiai,2 and Tsutomu Chiba1
Department of Gastroenterology & Endoscopic Medicine,1
Department of Pathology, Kyoto University, Sakyo, Kyoto, 606-8507, Japan2
Received 30 September 2002/
Returned for modification 25 November 2002/
Accepted 27 December 2002
We previously described an animal model of Helicobacter pylori-induced follicular gastritis in neonatally thymectomized (nTx) mice. However, it is still not clear whether antigen-presenting dendritic cells (DCs) in the stomach have a role in the development of secondary follicles in H. pylori-infected nTx mice. We investigated the distribution of DC subsets using this model and examined their roles. To identify lymphoid and myeloid DCs, sections were stained with anti-CD11c (pan-DC marker) in combination with anti-CD8
(lymphoid DC marker) or anti-CD11b (myeloid DC marker) and were examined with a confocal microscope. Expression of macrophage inflammatory protein 3
(MIP-3
), which chemoattracts immature DCs, was analyzed by real-time PCR and immunohistochemistry. Follicular dendritic cells (FDCs) were stained with anti-SKY28 antibodies. In noninfected nTx mice, a few myeloid and lymphoid DCs were observed in the bottom portion of the lamina propria, whereas in H. pylori-infected nTx mice, there was an increased influx of myeloid DCs throughout the lamina propria. FDC staining was also observed in the stomachs of members of the infected group. MIP-3
gene expression was upregulated in the infected nTx group, and the immunohistochemistry analysis revealed MIP-3
-positive epithelial cells. These data suggest that H. pylori infection upregulates MIP-3
gene expression in gastric epithelial cells and induces an influx of myeloid DCs in the lamina propria of the gastric mucosa in nTx mice. Myeloid DCs and FDCs might contribute to the development of gastric secondary lymphoid follicles in H. pylori-infected nTx mice.
* Corresponding author. Mailing address: Department of Gastroenterology & Endoscopic Medicine, Faculty of Medicine, Kyoto University, 54 Shogoin-Kawara-cho, Sakyo, Kyoto, 606-8507, Japan. Phone: 81-75-751-4319. Fax: 81-75-751-3414. E-mail:
okak{at}kuhp.kyoto-u.ac.jp.
Editor: A. D. O'Brien
Infection and Immunity, April 2003, p. 2153-2162, Vol. 71, No. 4
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.4.2153-2162.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
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