Leading article
The importance of interleukin 1
in
Helicobacter pylori associated
disease
| The first 150 words of the full text of this article appear below. |
| |
Introduction |
|---|
Helicobacter pylori infection is
associated with divergent clinical outcomes that range from simple
asymptomatic gastritis to more serious conditions such as peptic ulcer
disease and gastric neoplasia. The key determinants of these outcomes
are the severity and distribution of the H
pylori induced gastritis. Gastritis that is largely confined to
the antral region is associated with excessive acid secretion and a
high risk of duodenal ulcer disease.1 In contrast,
gastritis that involves the acid secreting corpus region leads to
hypochlorhydria, progressive gastric atrophy, and an increased risk of
gastric cancer.2 The association of H
pylori with such variable outcome poses a fascinating scientific challenge, the unravelling of which will not only explain how ulcers
and gastric cancer develop but will also act as a paradigm for
gene-environment interactions in most human diseases. The proinflammatory cytokine interleukin (IL)-1
is emerging as a key
mediator of many pathophysiological events that characterise
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