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Infection and Immunity, January 2006, p. 248-256, Vol. 74, No. 1
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.1.248-256.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Implications for Induction of Autoimmunity via Activation of B-1 Cells by Helicobacter pylori Urease

Shingo Yamanishi,1,2 Tadasu Iizumi,1 Eri Watanabe,1 Masumi Shimizu,1 Shigeru Kamiya,3 Kumiko Nagata,4 Yoshihiro Kumagai,1 Yoshitaka Fukunaga,2 and Hidemi Takahashi1*

Department of Microbiology and Immunology,1 Department of Pediatrics, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602,2 Department of Infectious Disease, Division of Medical Microbiology, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611,3 Department of Bacteriology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8131, Japan4

Received 18 August 2005/ Returned for modification 1 October 2005/ Accepted 13 October 2005

Besides various gastroduodenal diseases, Helicobacter pylori infection may be involved in autoimmune disorders like rheumatoid arthritis (RA) or idiopathic thrombocytopenic purpura. Such autoimmune disorders are often associated with autoreactive antibodies produced by B-1 cells, a subpopulation of B lymphocytes. These B-1 cells are mainly located in the pleural cavity or mucosal compartment. The existence of H. pylori urease-specific immunoglobulin A (IgA)-producing B cells in the mucosal compartment and of their specific IgM in the sera of acutely infected volunteers suggests the possibility that urease stimulates mucosal innate immune responses. Here, we show for the first time that purified H. pylori urease predominantly stimulates the B-1-cell population rather than B-2 cells, which produce antigen-specific conventional antibodies among splenic B220+ B cells. The fact that such stimulation of B-1 cells was not affected by the addition of polymyxin B indicates that the effect of purified H. pylori urease was not due to the contamination with bacterial lipopolysaccharide. Furthermore, the production of various B-1-cell-related autoreactive antibodies such as IgM-type rheumatoid factor, anti-single-stranded DNA antibody, and anti-phosphatidyl choline antibody was observed when the splenic B cells were stimulated with purified H. pylori urease in vitro. These findings suggest that H. pylori components, urease in particular, may be among the environmental triggars that initiate various autoimmune diseases via producing autoreactive antibodies through the activation of B-1 cells. The findings shown here offer important new insights into the pathogenesis of autoimmune disorders related to H. pylori infection.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan. Phone: 81-3-3822-2131, ext. 5381. Fax: 81-3-3316-1904. E-mail: htkuhkai{at}nms.ac.jp.

Editor: J. D. Clements

Infection and Immunity, January 2006, p. 248-256, Vol. 74, No. 1
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.1.248-256.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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