Is Helicobacter pylori infection protective against esophageal cancer?

Table 3 Mechanisms underlying the protective role of Helicobacter pylori infection against esophageal adenocarcinoma

Mechanism	Description	Implications
Development of atrophic gastritis	The inflammatory processes in chronic H. pylori infection can cause gastric atrophy by loss of gastric glands and partial replacement by intestinal epithelium. This reduces the number of parietal cells which secrete hydrochloric acid, the main constituent of gastric acid	Lower gastric acidity reduces the risk of GERD and BE, risk factors for EAC
Alteration of plasma ghrelin levels	H. pylori-induced gastric atrophy leads to reduced gastric ghrelin production, subsequently decreasing plasma ghrelin levels. Contrastingly, eradication of H. pylori increases ghrelin levels, thus leading to obesity. Thus, H. pylori infection is inversely related to obesity	Ghrelin is a key regulator of obesity and has been implicated in the pathogenesis and differentiation of esophageal cancers. Obesity can predispose individuals to GERD, which is a risk factor for both BE and EAC
Induction of cancer cell apoptosis	In vitro, H. pylori induces apoptosis in Barrett’s-derived EAC cells at a higher rate than in healthy esophageal cells. H. pylori activates the Fas-caspase cascade by increasing Fas protein expression in EAC cells, which leads to apoptosis through the fragmentation of cellular DNA	H. pylori infection can induce apoptosis and thus reduce the rate of esophageal cancer progression

H. pylori: Helicobacter pylori; GERD: Gastroesophageal reflux disease; BE: Barrett’s esophagus; EAC: Esophageal adenocarcinoma.