Journal
JOURNAL OF CLINICAL MICROBIOLOGY
Volume 39, Issue 4, Pages 1283-1288Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JCM.39.4.1283-1288.2001
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The Mongolian gerbil model For Helicobacter pylori infection is an animal model that mimics human disease. We examined the serum immune response to Ii. 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-wpathogen-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 oc 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 Ii pylori-related gastric lesions.
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