Next Article in Journal
Comprehensive Analysis of Prokaryotes in Environmental Water Using DNA Microarray Analysis and Whole Genome Amplification
Next Article in Special Issue
The Gastrointestinal Microbiome and Musculoskeletal Diseases: A Beneficial Role for Probiotics and Prebiotics
Previous Article in Journal
Culture-Independence for Surveillance and Epidemiology
Article Menu

Export Article

Open AccessArticle
Pathogens 2013, 2(4), 571-590;

Effects of EGFR Inhibitor on Helicobacter pylori Induced Gastric Epithelial Pathology in Vivo

Leeds Institute of Molecular Medicine, St. James's University Hospital, Leeds LS9 7TF, UK
Department of Pathology, University of Leeds, Leeds LS2 9JT, UK
Department of Gastroenterology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3GA, UK
Author to whom correspondence should be addressed.
Received: 13 August 2013 / Revised: 16 September 2013 / Accepted: 26 September 2013 / Published: 14 October 2013
(This article belongs to the Special Issue Gut Microbiome)
Full-Text   |   PDF [1655 KB, uploaded 14 October 2013]   |  


Helicobacter pylori transactivates the Epidermal Growth Factor Receptor (EGFR) and predisposes to gastric cancer development in humans and animal models. To examine the importance of EGFR signalling to gastric pathology, this study investigated whether treatment of Mongolian gerbils with a selective EGFR tyrosine kinase inhibitor, EKB-569, altered gastric pathology in chronic H. pylori infection. Gerbils were infected with H. pylori and six weeks later received either EKB-569-supplemented, or control diet, for 32 weeks prior to sacrifice. EKB-569-treated H. pylori-infected gerbils had no difference in H. pylori colonisation or inflammation scores compared to infected animals on control diet, but showed significantly less corpus atrophy, mucous metaplasia and submucosal glandular herniations along with markedly reduced antral and corpus epithelial proliferation to apoptosis ratios. EKB-569-treated infected gerbils had significantly decreased abundance of Cox-2, Adam17 and Egfr gastric transcripts relative to infected animals on control diet. EGFR inhibition by EKB-569 therefore reduced the severity of pre-neoplastic gastric pathology in chronically H. pylori-infected gerbils. EKB-569 increased gastric epithelial apoptosis in H. pylori-infected gerbils which counteracted some of the consequences of increased gastric epithelial cell proliferation. Similar chemopreventative strategies may be useful in humans who are at high risk of developing H.pylori-induced gastric adenocarcinoma. View Full-Text
Keywords: Helicobacter pylori; EGFR inhibitor; EKB-569; epithelial cell proliferation; apoptosis Helicobacter pylori; EGFR inhibitor; EKB-569; epithelial cell proliferation; apoptosis

Figure 1

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Crabtree, J.E.; Jeremy, A.H.; Duval, C.; Dixon, M.F.; Danjo, K.; Carr, I.M.; Pritchard, D.M.; Robinson, P.A. Effects of EGFR Inhibitor on Helicobacter pylori Induced Gastric Epithelial Pathology in Vivo. Pathogens 2013, 2, 571-590.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Pathogens EISSN 2076-0817 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top