Is Helicobacter pylori infection protective against esophageal cancer?

Abstract

Helicobacter pylori (H. pylori) infection affects a substantial proportion of the global population and causes various gastric disorders, including gastric cancer. Recent studies have found an inverse relationship between H. pylori infection and esophageal cancer (EC), suggesting a protective role against EC. This editorial focuses on the possible mechanisms underlying the role of H. pylori infection in EC and explores the role of gut microbiota in esophageal carcinogenesis and the practicality of H. pylori eradication. EC has two major subtypes: Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), which have different etiologies and risk factors. Gut microbiota can contribute to EC via inflammation-induced carcinogenesis, immunomodulation, lactagenesis, and genotoxin production. H. pylori infection is said to be inversely related to EAC, protecting against EAC by inducing atrophic gastritis, altering serum ghrelin levels, and triggering cancer cell apoptosis. Though H. pylori infection has no significant association with ESCC, COX-2-1195 polymorphisms and endogenous nitrosamine production can impact the risk of ESCC in H. pylori-infected individuals. There are concerns regarding a plausible increase in EC after H. pylori eradication treatments. However, H. pylori eradication is not associated with an increased risk of EC, making it safe from an EC perspective.