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Journal of Clinical Microbiology, April 2001, p. 1283-1288, Vol. 39, No. 4
0095-1137/01/$04.00+0   DOI: 10.1128/JCM.39.4.1283-1288.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Serum Immunoglobulin G Immune Response to Helicobacter pylori Antigens in Mongolian Gerbils

Toshiko Kumagai,1 Jing Yan,2 David Y. Graham,3,4 Minoru Tozuka,1 Yukie Okimura,1 Tatsuo Ikeno,5 Atsushi Sugiyama,5 Tsutomu Katsuyama,1,2 and Hiroyoshi Ota1,6,*

Central Clinical Laboratories1 and Department of Endoscopy,6 Shinshu University Hospital, and Department of Laboratory Medicine2 and First Department of Surgery,5 Shinshu University School of Medicine, Nagano 390-8621, Japan, and Departments of Medicine3 and Molecular Virology and Microbiology,4 Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas 77030

Received 31 July 2000/Returned for modification 21 October 2000/Accepted 11 January 2001

The Mongolian gerbil model for Helicobacter pylori infection is an animal model that mimics human disease. We examined the serum immune response to H. pylori infection in gerbils by enzyme-linked immunosorbent assay (ELISA) and Western blotting, both with whole-cell (H. pylori) extracts. A total of 66 7-week-old specific-pathogen-free male gerbils were inoculated orogastrically with H. pylori strain ATCC 43504. Sera were collected 1, 2, 4, 8, 12, 26, 38, and 52 weeks after H. pylori inoculation. Sixty-nine noninfected gerbils and their sera were used as controls. The specificity of the ELISA was 95.7%. The frequency of seropositivity increased over time: 2 of 10 (20%), 7 of 10 (70%), and 7 of 7 (100%) samples of sera from inoculated gerbils were positive for H. pylori at 2, 4, and 8 weeks postinoculation, respectively. Western blot assays showed that the primary immunoglobulin G (IgG) response against low-molecular-mass (25-, 30-, and 20-kDa) proteins appeared after a lag period of 2 to 8 weeks after inoculation. Antibodies against 160-, 150-, 110-, 120-, 80-, 66-, and 63-kDa proteins were observed 12 weeks after inoculation. The early reactive 30-kDa protein was identified as a urease alpha  subunit by N-terminal amino acid sequencing. After 26 weeks, two groups of animals could be distinguished: one group developed ulcers (n = 5), and the other developed hyperplastic polyps without ulcers (n = 19). Gerbils in the gastric ulcer group showed significantly higher serum anti-H. pylori IgG levels than did gerbils in the hyperplastic group (P = 0.001) as measured by ELISA. Furthermore, a higher proportion of animals developed antibodies to H. pylori proteins of 26, 25, and 20 kDa in the ulcer group than those animals with hyperplastic polyps (75 to 100% versus 17 to 50%) in Western blot assays. These results highlight the importance of the immune response of the host in the development of H. pylori-related gastric lesions.

* Corresponding author. Mailing address: Central Clinical Laboratories, Shinshu University Hospital, Asahi 3-1-1, Matsumoto, Nagano 390-8621, Japan. Phone: 81-263-35-4600 (ext. 5337). Fax: 81-263-34-5316. E-mail: hota{at}hsp.md.shinshu-u.ac.jp.

Journal of Clinical Microbiology, April 2001, p. 1283-1288, Vol. 39, No. 4
0095-1137/01/$04.00+0   DOI: 10.1128/JCM.39.4.1283-1288.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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