Interactions Between Intestinal Microbiota and Innate Immune System in Pediatric Inflammatory Bowel Disease

2012 ◽  
Vol 46 ◽  
pp. S64-S66 ◽  
Author(s):  
Salvatore Cucchiara ◽  
Laura Stronati ◽  
Marina Aloi
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune System ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Innate Immune System ◽  
Innate Immune ◽  
Pediatric Inflammatory Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Microbial Sensing by the Intestinal Epithelium in the Pathogenesis of Inflammatory Bowel Disease

2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Michael Scharl ◽  
Gerhard Rogler
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune System ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Innate Immune System ◽  
Pathogenic Bacteria ◽  
Intestinal Inflammation ◽  
Innate Immune ◽  
Model Systems ◽  
Inflammatory Bowel

Recent years have raised evidence that the intestinal microbiota plays a crucial role in the pathogenesis of chronic inflammatory bowels diseases. This evidence comes from several observations. First, animals raised under germ-free conditions do not develop intestinal inflammation in several different model systems. Second, antibiotics are able to modulate the course of experimental colitis. Third, genetic polymorphisms in a variety of genes of the innate immune system have been associated with chronic intestinal inflammatory diseases. Dysfunction of these molecules results in an inappropriate response to bacterial and antigenic stimulation of the innate immune system in the gastrointestinal tract. Variants of pattern recognition receptors such as NOD2 or TLRs by which commensal and pathogenic bacteria can be detected have been shown to be involved in the pathogenesis of IBD. But not only pathways of microbial detection but also intracellular ways of bacterial processing such as autophagosome function are associated with the risk to develop Crohn's disease. Thus, the “environment concept” and the “genetic concept” of inflammatory bowel disease pathophysiology are converging via the intestinal microbiota and the recognition mechanisms for an invasion of members of the microbiota into the mucosa.

Role of the Innate Immune System in the Pathogenesis of Inflammatory Bowel Disease

2009 ◽  
Vol 48 (2) ◽  
pp. 142-151 ◽  
Author(s):  
Pieter PE van Lierop ◽  
Janneke N Samsom ◽  
Johanna C Escher ◽  
Edward ES Nieuwenhuis
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune System ◽  
Bowel Disease ◽  
Innate Immune System ◽  
Innate Immune ◽  
Inflammatory Bowel

Extra-articular manifestations: inflammatory bowel disease

2016 ◽  
Author(s):  
Dirk Elewaut ◽  
Heleen Cypers ◽  
Matthew L. Stoll ◽  
Charles O. Elson
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Innate Immune ◽  
Intestinal Barrier Function ◽  
Innate Immune Responses ◽  
Susceptible Host ◽  
Inflammatory Bowel

A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.

Sign in / Sign up

Export Citation Format

Share Document