The goal of this study was to determine whether
Helicobacter pylori lipopolysaccharide (LPS) O-chain
polysaccharide contributes to
gastritis in a mouse model. C57BL/6J or C57BL/6-Prkdc(scid) (severe combined immunodeficient [SCID]) mice were inoculated with H. pylori strain SS1 or SS1::0826kan, in which a
beta-1,4-galactosyltransferase (HP0826), an LPS biosynthetic
enzyme, had been disrupted. H. pylori strain SS1::0826kan expresses truncated LPS lacking O chain. Recipient SCID mice were given C57BL/6J splenocytes by
intraperitoneal injection. Bacterial colonization, gastric lesions (
gastritis, neutrophilic infiltration, and gastric epithelial
metaplasia), cellular (delayed-type
hypersensitivity) and humoral immune responses to H. pylori sonicate, and gastric
gamma interferon (IFN-gamma)
mRNA expression were quantified. Recipient SCID mice colonized by H. pylori strain SS1 developed extensive
gastritis with loss of normal fundic gland morphology. In contrast, gastric mucosa of recipient SCID mice colonized by H. pylori strain SS1::0826kan was not statistically distinguishable from that of uninfected recipient mice. Delayed-type
hypersensitivity and humoral immune responses were detected in infected mice inoculated with wild-type SS1, but not with SS1::0826kan. IFN-gamma transcription was lower in mice infected with SS1::0826kan than in mice infected with SS1. In this model of rapidly progressive
gastritis due to H. pylori, the O chain contributed to the extent of
gastritis and to the host immune response. These data support a role for H. pylori LPS O chain in direct induction of the host immune response leading to
gastritis and gastric damage and are in contrast to
protein antigens, such as
urease and cag products which do not contribute to
gastritis in mice.