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World J Gastroenterol. Nov 14, 2014; 20(42): 15715-15726
Published online Nov 14, 2014. doi: 10.3748/wjg.v20.i42.15715
Published online Nov 14, 2014. doi: 10.3748/wjg.v20.i42.15715
Esophageal Helicobacter pylori colonization aggravates esophageal injury caused by reflux
Yun-Xiang Chu, Wei-Hong Wang, Yun Dai, Gui-Gen Teng, Shu-Jun Wang, Department of Gastroenterology, Peking University First Hospital, Beijing 100034, China
Author contributions: Chu YX and Wang WH contributed equally to this work; Chu YX performed the majority of experiments and wrote the manuscript; Wang WH designed the study and was involved in writing of the manuscript; Dai Y, Teng GG, and Wang SJ provided technical assistance; all of the authors read and approved the final version of the manuscript.
Supported by Grants from the National Natural Science Foundation of China, No. 81172271; and the Specialized Research Fund for the Doctoral Program of Higher Education, No. 20110001110064
Correspondence to: Wei-Hong Wang, Professor, Department of Gastroenterology, Peking University First Hospital, 8 Xishiku Avenue, Xicheng District, Beijing 100034, China. wangweihong@medmail.com.cn
Telephone: +86-10-83572616 Fax: +86-10-66518105
Received: January 30, 2014
Revised: April 22, 2014
Accepted: May 12, 2014
Published online: November 14, 2014
Revised: April 22, 2014
Accepted: May 12, 2014
Published online: November 14, 2014
Core Tip
Core tip: The relationship between gastroesophageal reflux disease and Helicobacter pylori (H. pylori) is controversial. This study demonstrates that esophageal H. pylori colonization can aggravate esophageal injury and promote the incidence of Barrett’s esophagus and esophageal adenocarcinoma. Gastric H. pylori colonization did not aggravate esophageal mucosal lesions in rats with mixed reflux. However, esophageal H. pylori infection was associated with increased cell proliferation and apoptosis in the esophagi of rats with mixed reflux. Loss of balance between cell proliferation and apoptosis may be important in H. pylori-induced esophageal malignancy.