Cukrowska B, Sowińska A, Bierła JB, Czarnowska E, Rybak A, Grzybowska-Chlebowczyk U. Intestinal epithelium, intraepithelial lymphocytes and the gut microbiota - Key players in the pathogenesis of celiac disease. World J Gastroenterol 2017; 23(42): 7505-7518 [PMID: 29204051 DOI: 10.3748/wjg.v23.i42.7505]
Corresponding Author of This Article
Bożena Cukrowska, MD, Professor, PhD, Department of Pathology, Laboratory of Immunology, The Children’s Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, Poland. b.cukrowska@ipczd.pl
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
Open-Access Policy of This Article
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/
World J Gastroenterol. Nov 14, 2017; 23(42): 7505-7518 Published online Nov 14, 2017. doi: 10.3748/wjg.v23.i42.7505
Intestinal epithelium, intraepithelial lymphocytes and the gut microbiota - Key players in the pathogenesis of celiac disease
Bożena Cukrowska, Agnieszka Sowińska, Joanna Beata Bierła, Elżbieta Czarnowska, Anna Rybak, Urszula Grzybowska-Chlebowczyk
Bożena Cukrowska, Agnieszka Sowińska, Joanna Beata Bierła, Elżbieta Czarnowska, Department of Pathology, The Children’s Memorial Health Institute, Warsaw 04-730, Poland
Anna Rybak, Department of Gastroenterology, Division of Neurogastroenterology and Motility, Great Ormond Street Hospital, London WC1N 3JH, United Kingdom
Urszula Grzybowska-Chlebowczyk, Department of Pediatrics, School of Medicine, Medical University of Silesia, Katowice, 40-752, Poland
Author contributions: Cukrowska B conceived and designed the study, and drafted and reviewed the manuscript; Sowińska A conceived the study, reviewed the literature, made the figures, and drafted the manuscript; Czarnowska E, Bierła J and Grzybowska-Chlebowczyk U reviewed the literature and drafted the manuscript; Rybak A drafted and reviewed the manuscript; all authors read and approved the manuscript.
Conflict-of-interest statement: The authors declare no conflicts of interest.
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/
Supported by the Children’s Memorial Health Institute Grants, No. 236/15, No. 243/16 and No. S147/2016.
Correspondence to: Bożena Cukrowska, MD, Professor, PhD, Department of Pathology, Laboratory of Immunology, The Children’s Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, Poland. b.cukrowska@ipczd.pl
Telephone: +48-2281-51091 Fax: +48-22815-1960
Received: May 22, 2017 Peer-review started: May 23, 2017 First decision: June 23, 2017 Revised: July 31, 2017 Accepted: August 15, 2017 Article in press: August 15, 2017 Published online: November 14, 2017 Processing time: 173 Days and 20 Hours
Core Tip
Core tip: There is evidence that the host-microbiota homeostasis is disrupted in celiac disease (CD) patients. Dysbiosis, meaning an imbalance in the gut microbiota and its metabolome, may activate innate immunity leading to pro-inflammatory changes, which induces intraepithelial lymphocyte infiltration and epithelial barrier damage, ultimately resulting in increased transfer of gluten peptides and inflammatory activation leading to CD development. The intestinal microbiota also has a direct effect on the breakdown of gluten and formation of immunogenic peptides. As colonization of the gut with microorganisms may be dependent on genetic factors, future prophylactic strategies may focus on gut microbiota modulation in genetically predisposed infants.
