Background: The inflammatory bowel diseases (IBD) are chronic relapsing inflammatory disorders of the gastrointestinal tract, comprising Crohn’s disease (CD), ulcerative colitis (UC), and IBD-unclassified (IBD-U). The microbiome, the barrier function, and the immune system play an integrated role in the development of IBD, and all three components are likely critical for perpetuating the disease process. Aims and project: In this study we have preliminary investigated some specific aspects of the IBD pathogenesis including the intestinal dysbiosis, the alteration of the intestinal barrier and the effect of a specific dietetic treatment (the so-called exclusive enteral nutrition, EEN). Methods: IBD pediatric patients were enrolled in the period 2013-2015. The study included 3 type of analysis: 1. Microbiota study: analysis of fecal microbiota in IBD in general (through the amplification of the V3-V4 regions of the 16S rRNA gene); 2. EEN study: evaluation of the clinical, laboratory and microbiological changes induced by EEN; 3. IPT study: evaluation of the intestinal barrier damage in IBD patients by the intestinal permeability test (IPT). Results: preliminary results of the microbiota study showed a different prevalence in some specific phyla in CD patients compared to UC. Such changes were not correlated to the level of inflammation. The results of the EEN study support the efficacy of EEN in the treatment of CD and preliminary results show a shift in microbiota composition after a course of EEN. IPT was found to be a sensitive test to detect disease activity and to evaluate response to treatments. Conclusion: Our study has generated novel and intriguing data especially with regards to microbiota changes secondary to EEN and to the modification of intestinal permeability following specific treatments.

Marcatori di danno intestinale nelle malattie infiammatorie croniche intestinali pediatriche / Gatti, Simona. - (2017 Mar 22).

Marcatori di danno intestinale nelle malattie infiammatorie croniche intestinali pediatriche

GATTI, SIMONA
2017-03-22

Abstract

Background: The inflammatory bowel diseases (IBD) are chronic relapsing inflammatory disorders of the gastrointestinal tract, comprising Crohn’s disease (CD), ulcerative colitis (UC), and IBD-unclassified (IBD-U). The microbiome, the barrier function, and the immune system play an integrated role in the development of IBD, and all three components are likely critical for perpetuating the disease process. Aims and project: In this study we have preliminary investigated some specific aspects of the IBD pathogenesis including the intestinal dysbiosis, the alteration of the intestinal barrier and the effect of a specific dietetic treatment (the so-called exclusive enteral nutrition, EEN). Methods: IBD pediatric patients were enrolled in the period 2013-2015. The study included 3 type of analysis: 1. Microbiota study: analysis of fecal microbiota in IBD in general (through the amplification of the V3-V4 regions of the 16S rRNA gene); 2. EEN study: evaluation of the clinical, laboratory and microbiological changes induced by EEN; 3. IPT study: evaluation of the intestinal barrier damage in IBD patients by the intestinal permeability test (IPT). Results: preliminary results of the microbiota study showed a different prevalence in some specific phyla in CD patients compared to UC. Such changes were not correlated to the level of inflammation. The results of the EEN study support the efficacy of EEN in the treatment of CD and preliminary results show a shift in microbiota composition after a course of EEN. IPT was found to be a sensitive test to detect disease activity and to evaluate response to treatments. Conclusion: Our study has generated novel and intriguing data especially with regards to microbiota changes secondary to EEN and to the modification of intestinal permeability following specific treatments.
22-mar-2017
ibd; crohn; microbiota; intestinal barrier; enteral nutrition
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11566/245512
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