1,721,006 research outputs found

    Epidemiology, genes and inflammatory bowel diseases in childhood

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    There is evidence that inflammatory bowel disease is immunologically mediated and that genetic factors play an important aetiological role. The identification of disease susceptibility genes has led to significant progress in our understanding of the pathogenesis of Crohn's disease. Genes linked to Crohn's disease play critical roles in the normal function of the innate immune system, and genes linked to epithelial integrity may play a role in the pathogenesis of inflammatory bowel disease as well. However, the dynamic epidemiology of both Crohn's disease and ulcerative colitis suggests that extrinsic environmental factors acting at the population level may be involved in their pathogenesis. These environmental factors may be responsible for the rising incidence of inflammatory bowel diseas

    Gut microbiota and pediatric disease

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    Background: Researchers have made every effort to assess the role of gut microbiota in pediatric diseases like inflammatory bowel disease (IBD), celiac disease, asthma, allergy, and autism. The leading hypothesis is that an altered microbial composition is present (other than the presence of a specific pathogen) and that it could be involved in the pathogenesis or progression of such disorders. Methods: Cultural, molecular, metabolomic, and metagenomic approaches are trying to define the pediatric gut microbiota imbalances in different diseases. Results and Conclusion: In pediatric IBD, a marked increase in aerobes and facultative anaerobes was found, along with an increase in Enterobacteriaceae members (Escherichia coli). In both pediatric IBD and celiac disease (Th1-mediated disorders), higher bacterial cell counts were observed, jointly with a general gain of biodiversity. A preponderance of Bacteroidetes and a parallel decrease of Firmicutes was also reported in IBD, celiac disease and autism. Contrarily, dietary changes due to Western lifestyles increase Firmicutes populations and lower short-chain fatty acids production, possibly exposing 'developed' children to the infectious challenge (Escherichia and Shigella spp.). Lactobacillus and Bifidobacterium species could be protective agents for atopic diseases, while Clostridia, Enterobacteriaceae, and staphylococci can be associated with an increased risk of such Th2-mediated disorders. In the brain-gut axis view, gut microbiota could also play a role in autism. Copyright (C) 2011 S. Karger AG, Base

    Endoplasmic reticulum stress and unfolded protein response are involved in paediatric inflammatory bowel disease

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    Endoplasmic reticulum stress and unfolded protein response have been recently associated with the development of inflammatory bowel diseases in adults. We aimed at assessing the involvement of these pathways also in paediatric inflammatory bowel disease by analysing the expression of the main genes involved in endoplasmic reticulum stress and correlating them with the degree of intestinal inflammation. Real-time PCR and Western blot analysis of the expression of the endoplasmic reticulum stress marker HSPA5 and of selected genes representing the three pathways of unfolded protein response (IRE-XBP1, PERK-ATF4, ATF6p90-p50) in inflamed and uninflamed biopsies from 28 inflammatory bowel disease paediatric patients and 10 controls. HSPA5, PDIA4, as well as unspliced and spliced XBP1 mRNAs were significantly increased in patients' inflamed colonic mucosa compared to uninflamed mucosa and controls. HSPA5, PDIA4, ATF6, and phospho-IRE proteins were also upregulated, indicating the activation of the IRE-XBP1 and ATF6p90-p50 branches of unfolded protein response. A positive significant correlation between interleukin-8 levels, as a marker of inflammation, and upregulated genes was found in the inflamed colonic mucosa. A deregulation of the genes involved in the endoplasmic reticulum stress and unfolded protein response pathways may be a key component of the inflammatory response in paediatric patients with inflammatory bowel disease
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