The host immune response to Helicobacter pylori infection might be of impor
tance with regard to the outcome of infection by this organism, e.g., to ex
plain why only a proportion of infected subjects develop peptic ulcers. In
this study we have analyzed the local response of different cytokines-i.e.,
the proinflammatory interleukin-1 beta, (IL-1 beta), IL-6, tumor necrosis
factor alpha, and IL-8; the immunoregulatory gamma interferon (IFN-gamma);
and IL-4; and the anti-inflammatory transforming growth factor beta (TGF-be
ta)-in antral biopsy specimens from H. pylori-infected duodenal deer (DU) p
atients and asymptomatic (AS) carriers (i.e., with chronic gastritis only).
For comparison, biopsy specimens from uninfected healthy individuals were
also analyzed. An immunohistochemical technique was used to allow quantific
ation of the cytokine responses as well as identification of the cell types
associated with the cytokine expression. We found that the levels of all o
f the studied cytokines except IL-4 were increased in the H. pylori-infecte
d subjects compared to the levels in the healthy individuals. Our results i
ndicate that the antral cytokine response is of the Th, type since IFN-gamm
a, but not IL-4, was up-regulated bath in H. pylori-infected DU patients an
d in AS carriers. However, there were no significant differences in either
proinflammatory or immunoregulatory cytokine levels when H. pylori-infected
subjects with and without peptic ulcers were compared. Some of the cytokin
es, particularly IL-1 beta and TGF-beta, were also found in the gastric muc
osae of healthy, uninfected subjects. We also showed that the gastric epith
elium contributes substantially to the antral cytokine response of the proi
nflammatory cytokines IL-1 beta and IL-6 in addition to IL-8.