Chamaillard M, Dessein R. Defensins couple dysbiosis to primary immunodeficiency in Crohn’s disease. World J Gastroenterol 2011; 17(5): 567-571 [PMID: 21350705 DOI: 10.3748/wjg.v17.i5.567]
Corresponding Author of This Article
Mathias Chamaillard, PhD, Institut Pasteur de Lille, Center for Infection and Immunity of Lille, 1, rue du Professeur Calmette, F-59019 Lille, France. mathias.chamaillard@inserm.fr
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World J Gastroenterol. Feb 7, 2011; 17(5): 567-571 Published online Feb 7, 2011. doi: 10.3748/wjg.v17.i5.567
Defensins couple dysbiosis to primary immunodeficiency in Crohn’s disease
Mathias Chamaillard, Rodrigue Dessein
Mathias Chamaillard, Rodrigue Dessein, Institut Pasteur de Lille, Center for Infection and Immunity of Lille, F-59019 Lille, France
Mathias Chamaillard, Rodrigue Dessein, CNRS, UMR 8204, F-59021 Lille, France
Mathias Chamaillard, Rodrigue Dessein, Institut National de la Santé et de la Recherche Médicale, U1019, Team 7, Equipe FRM, F-59019 Lille, France
Mathias Chamaillard, Rodrigue Dessein, Univ Lille Nord de France, F-59000 Lille, France
Rodrigue Dessein, C.H.R.U. de Lille, F-59000 Lille, France
Author contributions: Chamaillard M and Dessein R wrote the paper.
Correspondence to: Mathias Chamaillard, PhD, Institut Pasteur de Lille, Center for Infection and Immunity of Lille, 1, rue du Professeur Calmette, F-59019 Lille, France. mathias.chamaillard@inserm.fr
Telephone: +33-3-59317427 Fax: +33-3-59317480
Received: May 8, 2010 Revised: June 4, 2010 Accepted: June 11, 2010 Published online: February 7, 2011
Abstract
Antimicrobial peptides, including defensins, are essential effectors in host defence and in the maintenance of immune homeostasis. Clinical studies have linked the defective expression of both α- and β-defensin to the reduced killing of certain microorganisms by the intestinal mucosa of patients suffering from ileal and colonic Crohn’s disease (CD), respectively. Only recently have the events leading to defective expression of defensins in CD been further elucidated, and are discussed herein. These events may account for CD-associated alterations in the microbiome and may subsequently precipitate the development of granulomatous inflammatory lesions in genetically-predisposed patients. We also address how these discoveries may pave the way for the development of a molecular medicine aimed at restoring gut barrier function in CD.
