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Infection and Immunity, January 1999, p. 279-285, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Role of Gamma Interferon in Helicobacter pylori-Induced Gastric Inflammatory Responses in a Mouse Model

Naoki Sawai,1,* Masakazu Kita,2 Tadashi Kodama,1 Toshihito Tanahashi,1 Yoshio Yamaoka,1 Yoh-ichi Tagawa,3 Yoichiro Iwakura,3 and Jiro Imanishi2

Third Department of Internal Medicine1 and Department of Microbiology,2 Kyoto Prefectural University of Medicine, Kyoto 602-0841, and Laboratory Animal Research Center, Institute of Medical Science, University of Tokyo, Tokyo 108-8639,3 Japan

Received 28 May 1998/Returned for modification 29 July 1998/Accepted 22 October 1998

The immune responses to Helicobacter pylori infection play important roles in gastroduodenal diseases. The contribution of gamma interferon (IFN-gamma ) to the immune responses, especially to the induction of gastric inflammation and to protection from H. pylori infection, was investigated with IFN-gamma gene knockout (IFN-gamma -/-) mice. We first examined the colonizing abilities of eight H. pylori strains with a short-term infection test in order to select H. pylori strains which could colonize the mouse stomach. Only three strains (ATCC 43504, CPY2052, and HPK127) colonized C57BL/6 wild-type mice, although all of the strains except for ATCC 51110 could colonize IFN-gamma -/- mice. The number of H. pylori organisms colonizing the stomach in wild-type mice was lower than that in IFN-gamma -/- mice. Oral immunization with the CPY2052 sonicate and cholera toxin protected against infection with strain CPY2052 in both types of mouse. These findings suggested that IFN-gamma may play a protective role in H. pylori infection, although the degree of its protective ability was estimated to be low. In contrast, in a long-term infection test done to examine the contribution of IFN-gamma to gastric inflammation, CPY2052-infected wild-type mice developed a severe infiltration of mononuclear cells in the lamina propria and erosions in the gastric epithelium 15 months after infection, whereas CPY2052-infected IFN-gamma -/- mice showed no inflammatory symptoms. This result clearly demonstrated that IFN-gamma plays an important role in the induction of gastric inflammation caused by H. pylori infection.

* Corresponding author. Mailing address: Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kawaramachi, Hirokoji, Kamigyo-ku, Kyoto 602-0841, Japan. Phone: 81-75-251-5519. Fax: 81-75-251-0710. E-mail: sawai{at}basic.kpu-m.ac.jp.

Infection and Immunity, January 1999, p. 279-285, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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