Review
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World J Gastrointest Pathophysiol. Feb 15, 2015; 6(1): 1-12
Published online Feb 15, 2015. doi: 10.4291/wjgp.v6.i1.1
Pathogenesis of Crohn’s disease: Bug or no bug
Marta Maia Bosca-Watts, Joan Tosca, Rosario Anton, Maria Mora, Miguel Minguez, Francisco Mora
Marta Maia Bosca-Watts, Joan Tosca, Rosario Anton, Maria Mora, Miguel Minguez, Francisco Mora, IBD Unit, Digestive Disease Department, University of Valencia, University Clinic Hospital of Valencia and INCLIVA Health Research Institute, 46010 Valencia, Spain
Author contributions: All authors contributed equally in the review of the medical literature and in writing the article; Bosca-Watts MM led the organization of the research and translated the final document from Spanish to English; Minguez M and Mora F supervised and corrected the review.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Marta Maia Bosca-Watts, MD, IBD Unit, Digestive Disease Department, University of Valencia, University Clinic Hospital of Valencia and INCLIVA Health Research Institute, Avda. Blasco Ibañez 17, 46010 Valencia, Spain. inflamatoriahcuv@gmail.com
Telephone: +34-96-1973500 Fax: +34-96-1973500
Received: May 17, 2014
Peer-review started: May 18, 2014
First decision: June 18, 2014
Revised: November 1, 2014
Accepted: November 7, 2014
Article in press: November 10, 2014
Published online: February 15, 2015
Processing time: 260 Days and 1.6 Hours
Abstract

The possibility of an infectious origin in inflammatory bowel disease (IBD) has been postulated since the first description of Crohn’s disease (CD). Many observations implicate bacteria as a trigger for the development of CD: lesions occur in regions with higher bacterial concentrations; aphthous ulcers occur in Peyer’s patches; inflammation resolves when the fecal stream is diverted and is reactivated following reinfusion of bowel contents; severity of the disease is correlated with bacterial density in the mucosa; granulomas can contain bacteria; and susceptible mice raised in germ-free conditions develop inflammation when bacteria are introduced in the 1990’s, several studies sought to establish a relationship with viral infections and the onset of IBD, finally concluding that no direct link had been demonstrated. In the past fifteen years, evidence relating IBD pathogenesis to Mycobacterium avium paratuberculosis, salmonella, campylobacter, etc., has been found. The tendency now under discussion to regard microbiota as the primary catalyst has led to the latest studies on microbiota as pathogens, focusing on Escherichia coli, mainly in ileal CD. The present review discusses the literature available on these “bugs”.

Keywords: Inflammatory bowel disease; Crohn’s disease; Ulcerative colitis; Bacteria; Virus; Pathogenesis

Core tip: The possibility of an infectious origin in inflammatory bowel disease (IBD) has been postulated since the first description of Crohn’s disease (CD). Many observations implicate bacteria as a trigger for the development of CD, and have tried to do so with virus. Inconclusive evidence relating IBD pathogenesis to Mycobacterium avium paratuberculosis, salmonella, campylobacter, etc., has been found. The tendency now under discussion to regard microbiota as the primary catalyst, has led to the latest studies on microbiota as pathogens, focusing on Escherichia coli, mainly in ileal CD. The present review discusses the literature available on these “bugs”.