Effect of Helicobacter pylori Infection on Barrett’s Esophagus and Esophageal Adenocarcinoma Formation in a Rat Model of Chronic Gastroesophageal Reflux

Abstract

When H. pylori infect in stomach, it may reduce the severity of inflammation. However, when colonizes in esophagus, H. pylori increases the severity of esophageal inflammation and the incidence of BE and EA. Celecoxib administration attenuates the incidence of EA by inhibiting COX-2 expression.

Carcinogenesis of Barrett’s esophagus: a review of the clinical literature

“…In contrast, in a rat model of chronic gastroesophageal reflux, when H. pylori colonized in the esophagus, the bacteria increased the severity of esophageal inflammation and the incidence of BE and EAC [84].…”

“…In another study, patients with EAC used NSAIDs/aspirin more frequently compared to the controls (OR 1.8, 95 % CI 1.1-3.2) [131]. In contrast, celecoxib treatment attenuated the incidence of EAC by inhibiting COX-2 expression in an animal model [84]. The possible beneficial role of NSAIDs/aspirin needs to be further examined, with special attention to the progression from BE to cancer.…”

Ki-67 and Bax expression in esophageal mucosa might have implications in ablative therapies for Barrett’s esophagus, dysplasia, and adenocarcinoma

“…When H. pylori colonizes the esophagus, the severity of esophageal inflammation and the incidence of BE and EA are increased [13]. In this respect, our own and other relative data show that H. pylori is frequent in GERD, even in nonendoscopic reflux disease and BE [9][10][11], and H. pylori eradication leads to a better control of GERD symptoms and improves esophagitis [12].…”

“…Another, still controversial, issue, Helicobacter pylori infection may be involved in the GERD-BE-EA sequence and its eradication might inhibit the progress of this sequence [8][9][10][11][12][13][14]. When H. pylori colonizes the esophagus, the severity of esophageal inflammation and the incidence of BE and EA are increased [13].…”

Reply to Letter to the Editor: Re: Comparison of COX-2, Ki-67, and BCL-2 expression in normal esophageal mucosa, Barrett’s esophagus, dysplasia, and adenocarcinoma with postablation mucosa and implications for ablative therapies (Online First)

“…We note that the cited study relating the higher levels of COX-2 expression and prostaglandin E2 with esophageal H. pylori colonization was based purely on an animal model [15]. Despite the various organic similarities between such animals and humans, including the activation of common genetic pathways, role of hypergastrinemia, and duodenogastric reflux in cancer progression, such animal studies do not necessarily reflect the equivalent pattern of human disease [16].…”