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Defining dysbiosis threatens Koch's postulates and current dogma on the role of Paneth cells in Crohn's disease
  1. Mathias Chamaillard,
  2. Katarina Radulovic
  1. University of Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019, UMR 8204, CIIL, Centre d'Infection et d'Immunité de Lille, F-59000 Lille, France
  1. Correspondence to Dr Mathias Chamaillard, Institut National de la Santé et de la Recherche Médicale, U1019, Lille F-59019, France; mathias.chamaillard{at}inserm.fr

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Whereas the intestinal epithelium self-renews every 3–5 days, it promotes a robust antimicrobial response to enteropathogens when they first breach the integrity of the mucosal barrier. Foremost, the interaction between gut commensals and the single layer of intestinal epithelial cells is involved in many common, essential physiological processes (eg, nutrient absorption, cell proliferation, cell motility and metabolic activities). In Crohn's disease, it is thought that impaired epithelial function develops into transmural inflammatory lesions at the terminal ileum, where abnormal granule formation and enhanced necroptosis of Paneth cells are frequently observed. Located at the base of the crypt of Lieberkühn in the small intestine, Paneth cells are one of the four major epithelial cell lineages, which play an essential role in maintaining the resistance of epithelial surfaces to microbial colonisation. Accordingly, genome-wide association studies have revealed a large set of inborn genetic errors in several regulatory factors involved in the maintenance of Paneth cell function.1 However, it is still not clear whether impaired secretory function of Paneth cell precedes the onset and relapse of Crohn's disease. In this context, it is essential to gain an understanding of the exact …

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