Esophageal adenocarcinoma develops through a cascade of cellular changes that shares similarities to the etiology of Helicobacter pylori-associated intestinal-type gastric adenocarcinoma. While host genetics and immune response have been implicated in the progression to esophageal adenocarcinoma, studies investigating esophageal microbial communities suggest that bacteria may also play an important role in driving the inflammation that leads to disease. Of these, emerging Campylobacter species have been found to be more prevalent and abundant in patients progressing through the esophageal adenocarcinoma cascade compared to controls. Given that these bacteria possess several virulence mechanisms such as toxin production, cellular invasion, and intracellular survival, emerging Campylobacter species should be investigated as etiological agents of the chronic esophageal inflammation that leads to cancer.
Keywords: Barrett's esophagus; Campylobacter concisus; Helicobacter pylori; esophageal adenocarcinoma; gastric adenocarcinoma; gastro-esophageal reflux disease.
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