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J. Exp. Med., Volume 188, Number 12, December 21, 1998 2277-2288

Immunization of Mice with Urease Vaccine Affords Protection against Helicobacter pylori Infection in the Absence of Antibodies and Is Mediated by MHC Class II-restricted Responses

By Thomas H. Ermak,* Paul J. Giannasca,* Richard Nichols,* Gwendolyn A. Myers,* John Nedrud,Dagger Richard Weltzin,* Cynthia K. Lee,* Harold Kleanthous,* and Thomas P. Monath*

From * OraVax, Inc., Cambridge, Massachusetts 02139; and Dagger  Case Western Reserve University, Cleveland, Ohio 44106

We examined the roles of cell- and antibody-mediated immunity in urease vaccine-induced protection against Helicobacter pylori infection. Normal and knockout mice deficient in major histocompatibility complex (MHC) class I, MHC class II, or B cell responses were mucosally immunized with urease plus Escherichia coli heat-labile enterotoxin (LT), or parenterally immunized with urease plus aluminum hydroxide or a glycolipid adjuvant, challenged with H. pylori strain X47-2AL, and H. pylori organisms and leukocyte infiltration in the gastric mucosa quantified. In an adjuvant/route study in normal mice, there was a direct correlation between the level of protection and the density of T cells recruited to the gastric mucosa. In knockout studies, oral immunization with urease plus LT protected MHC class I knockout mice [beta 2-microglobulin (-/-)] but not MHC class II knockout mice [I-Ab (-/-)]. In B cell knockout mice [µMT (-/-)], vaccine-induced protection was equivalent to that observed in immunized wild-type (+/+) mice; no IgA+ cells were detected in the stomach, but levels of CD4+ cells equivalent to those in the wild-type strain (+/+) were seen. These studies indicate that protection of mice against H. pylori infection by immunization with the urease antigen is dependent on MHC class II-restricted, cell-mediated mechanisms, and antibody responses to urease are not required for protection.

Key words: Helicobacter pylori;  knockout mice;  adjuvants;  gastric mucosa;  T cells


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