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World J Gastroenterol. Jul 21, 2014; 20(27): 8751-8763
Published online Jul 21, 2014. doi: 10.3748/wjg.v20.i27.8751
Published online Jul 21, 2014. doi: 10.3748/wjg.v20.i27.8751
Escherichia coli-host macrophage interactions in the pathogenesis of inflammatory bowel disease
Ahmed Tawfik, Paul K Flanagan, Barry J Campbell, Department of Gastroenterology, Institute of Translational Medicine, University of Liverpool, Liverpool L69 3GE, United Kingdom
Author contributions: The review was proposed by Campbell BJ; Tawfik A, Flanagan PK and Campbell BJ drafted the initial manuscript; Campbell BJ reviewed and edited the draft; all authors approved the final manuscript before submission.
Supported by Award from the Ministry of Higher Education and Scientific Research/Cultural Attache - London Libyan Embassy, No. UM873-611-23962; National Institute for Health Research (NIHR) Biomedical Research Fellowship, No. BRF-2011-025; Shire Innovation Fund for Specialist Registrars; and funding from Crohn’s amd Colitis United Kingdom, No. M-08-1/M-13-2; Liverpool NIHR-Biomedical Research Centre for Microbial Diseases (01CD1); and Support of the European Science Foundation, in the framework of the Research Networking Programme, The European Network for Gastrointestinal Health Research
Correspondence to: Dr. Barry J Campbell, Department of Gastroenterology, Institute of Translational Medicine, University of Liverpool, Nuffield Building, Crown Street, Liverpool, L69 3GE, United Kingdom. bjcampbl@liv.ac.uk
Telephone: +44-151-7946829 Fax: +44-151-7946825
Received: October 22, 2013
Revised: January 7, 2014
Accepted: April 1, 2014
Published online: July 21, 2014
Revised: January 7, 2014
Accepted: April 1, 2014
Published online: July 21, 2014
Core Tip
Core tip: There is significant evidence implicating adherent, invasive mucosa-associated Escherichia coli (AIEC) in the pathogenesis of Crohn’s disease. AIEC translocate M-cells of Peyer’s patches and lymphoid follicles of the colon, and then to survive and replicate within underlying mucosal macrophages. How Crohn’s AIEC resist killing and adapt to the environment within the phagolysosme to survive and grow within macrophages is still poorly understood. Here we review the current understanding of the role of AIEC in Crohn’s pathogenesis, the role of the innate immune system, factors which may contribute to prolonged bacterial survival and therapeutic strategies to target intracellular AIEC.