Protective effects of Helicobacter pylori against gastroesophageal reflux disease may be due to a neuroimmunological anti-inflammatory mechanism

There is some evidence that Helicobacter pylori infection has a protective effect against gastroesophageal reflux disease (GORD)
and its complications such as Barrett’s oesophagus and oesophageal adenocarcinoma. In this paper, we propose that a
neuroimmunological mechanism is responsible for the protective effect of H. pylori on GORD. H. pylori infection of the gastric
mucosa induces a T helper1-like immune response and production of pro-inflammatory cytokines. These cytokines can inhibit
local sympathetic tone, whereas they increase systemic sympathetic tone. Increased sympathetic tone can induce an antiinflammatory
milieu, which in turn can inhibit inflammation in the oesophagus and lower oesophageal sphincter (LOS).
Furthermore, H. pylori infection may stimulate the cholinergic anti-inflammatory pathway. It has been suggested that refluxinduced
oesophageal inflammation plays an important role in the pathogenesis of reflux oesophagitis. Reduction of oesophageal
inflammation by increased systemic sympathetic tone and vagal activity may lead to a decrease in reflux-induced oesophageal
injury and LOS dysfunction in GORD.