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J. Exp. Med.,
Volume 187, Number 10, May 18, 1998 1659-1669
By
¶
From the * Department of Pediatrics, the Helicobacter pylori infection is associated with gastric epithelial damage, including apoptosis, ulceration, and cancer. Although bacterial factors and the host response are believed to contribute to gastric disease, no receptor has been identified that explains how the bacteria attach and
signal the host cell to undergo apoptosis. Using H. pylori as "bait" to capture receptor proteins
in solubilized membranes of gastric epithelial cells, class II major histocompatibility complex
(MHC) molecules were identified as a possible receptor. Signaling through class II MHC molecules leading to the induction of apoptosis was confirmed using cross-linking IgM antibodies to surface class II MHC molecules. Moreover, binding of H. pylori and the induction of apoptosis were inhibited by antibodies recognizing class II MHC. Since type 1 T helper cells are
present during infection and produce interferon (IFN)- Department of Microbiology and Immunology, the § Department of Internal Medicine, the Department of Pathology, and the ¶ Sealy Center for Molecular
Sciences, University of Texas Medical Branch, Galveston, Texas 77555
, which increases class II MHC expression, gastric epithelial cell lines were exposed to H. pylori in the presence or absence of
IFN-. IFN- increased the attachment of the bacteria as well as the induction of apoptosis in
gastric epithelial cells. In contrast to MHC II-negative cell lines, H. pylori induced apoptosis in
cells expressing class II MHC molecules constitutively or after gene transfection. These data
describe a novel receptor for H. pylori and provide a mechanism by which bacteria and the host
response interact in the pathogenesis of gastric epithelial cell damage.
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