27,286 research outputs found

    Cutaneous Manifestations in Inflammatory Bowel Diseases

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    Inflammatory bowel diseases have a high frequency in Europe. They are chronic disorders that evolve with relapses and remissions. Clinical features include the signs of underlying inflammatory bowel disease and also signs of extraintestinal manifestations. Cutaneous disorders are the most common extraintestinal manifestations associated with inflammatory bowel diseases, which can be dependent on or independent of gastrointestinal disease activity. The main cutaneous disorders are erythema nodosum and pyodermagangrenosum. The pathogenic mechanisms are not fully understood but it seems that related mechanisms are involved in the development of inflammatory bowel diseases and extraintestinal manifestations. Treatment should be aimed at both the cutaneous manifestations and the bowel inflammation

    Systems biology in inflammatory bowel diseases

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    Purpose of review: Ulcerative colitis (UC) and Crohn’s Disease (CD) are the two predominant types of inflammatory bowel disease (IBD), affecting over 1.4 million individuals in the US. IBD results from complex interactions between pathogenic components, including genetic and epigenetic factors, the immune response and the microbiome through an unknown sequence of events. The purpose of this review is to describe a system biology approach to IBD as a novel and exciting methodology aiming at developing novel IBD therapeutics based on the integration of molecular and cellular "omics" data. Recent Findings: Recent evidence suggested the presence of genetic, epigenetic, transcriptomic, proteomic and metabolomic alterations in IBD patients. Furthermore, several studies have shown that different cell types, including fibroblasts, epithelial, immune and endothelial cells together with the intestinal microbiota are involved in IBD pathogenesis. Novel computational methodologies have been developed aiming to integrate high - throughput molecular data. Summary: A systems biology approach could potentially identify the central regulators (hubs) in the IBD interactome and improve our understanding of the molecular mechanisms involved in IBD pathogenesis. The future IBD therapeutics should be developed on the basis of targeting the central hubs in the IBD network

    Smoking in inflammatory bowel diseases: Good, bad or ugly?

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    Smoking is an important environmental factor in inflammatory bowel disease (IBD), having different effects in ulcerative colitis (UC) and Crohn’s disease (CD). A recent meta-analysis partially confirmed previous findings that smoking was found to be protective against ulcerative colitis and, after onset of the disease, might improve its course, decreasing the need for colectomy. However, smoking increases the risk of developing Crohn’s disease and worsens its course, increasing the need for steroids, immunosuppressants and re-operations. Smoking cessation aggravates ulcerative colitis and improves Crohn’s disease. Data are however, largely conflictive as well as the potential mechanisms involved in this dual relationship are still unknown. In this review article, the authors review the role of smoking in inflammatory bowel diseases

    Pathogenesis of Inflammatory Bowel Diseases

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    Correlation Between Low Bone Density and Disease Activity in Patients with Ulcerative Colitis

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    BACKGROUND Different clinical and epidemiological studies using dual-energy X-ray absorptiometry have shown an increased prevalence of low bone mineral density in patients with inflammatory bowel diseases. The aim of this study was to assess the correlation between bone density and the disease activity in patient swith ulcerative colitis.KEYWORDS Ulcerative colitis; Z-score; Bone densitometry; Low bone densit

    Use of Animal Models in the Study of Colitis

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    Inflammatory bowel diseases (IBDs) relate to chronic inflammations in different parts of the gastrointestinal (GI) tract involving both ulcerative colitis (UC) and Crohn’s disease (CD). Ulcerative colitis begins in the rectum and extends continuously up the colon. Notably, CD may affect any area of the GIT, from the mouth to the anus. Various conditions may influence the genesis of the disease, such as genetics, environment, intestinal microbiota and the presence of agents of enteric infections. Experimental models are therefore suitably used to investigate the various etiological factors; similarly colitis can be induced by genetic modification, cell transfer, spontaneous inflammation and chemical agents. The objective of this chapter is to present current concept on animal models of inflammatory bowel diseases. These models are crucial for the understanding of inflammatory bowel diseases, development of alternative treatments and more effective therapeutic agents thus contributing to the control of the disease

    Ly49E Expression on CD8αα-expressing intestinal intraepithelial lymphocytes plays no detectable role in the development and progression of experimentally induced inflammatory bowel diseases

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    The Ly49E NK receptor is a unique inhibitory receptor, presenting with a high degree of conservation among mouse strains and expression on both NK cells and intraepithelial-localised T cells. Amongst intraepithelial-localised T cells, the Ly49E receptor is abundantly expressed on CD8 alpha alpha-expressing innate-like intestinal intraepithelial lymphocytes (iIELs), which contribute to front-line defense at the mucosal barrier. Inflammatory bowel diseases (IBDs), encompassing Crohn's disease and ulcerative colitis, have previously been suggested to have an autoreactive origin and to evolve from a dysbalance between regulatory and effector functions in the intestinal immune system. Here, we made use of Ly49E-deficient mice to characterize the role of Ly49E receptor expression on CD8 alpha alpha-expressing iIELs in the development and progression of IBD. For this purpose we used the dextran sodium sulphate (DSS)- and trinitrobenzenesulfonic-acid (TNBS)-induced colitis models, and the TNF Delta ARE ileitis model. We show that Ly49E is expressed on a high proportion of CD8 alpha alpha-positive iIELs, with higher expression in the colon as compared to the small intestine. However, Ly49E expression on small intestinal and colonic iIELs does not influence the development or progression of inflammatory bowel diseases

    Probiotics Can Cure Oral Aphthous-Like Ulcers in Inflammatory Bowel Disease Patients: A Review of the Literature and a Working Hypothesis

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    Dysbiosis has been associated with the onset of several chronic autoimmune or inflammatory pathologies (e.g., inflammatory bowel diseases-IBD), because of its primary role in the establishment of a chronic inflammatory process leading to tissue damage. Inflammatory bowel diseases can even involve areas far away from the gut, such as the extraintestinal manifestations involving the oral cavity with the onset of aphthous-like ulcers (ALU). Studies carried out on animal models have shown that intestinal dysbiosis may be related to the development of autoimmune diseases, even if the mechanisms involved are not yet well known. The aim of this paper is to verify the hypothesis that in inflammatory bowel diseases patients, aphthous-like ulcers are the result of the concomitance of intestinal dysbiosis and other events, e.g., the microtraumas, occurring in the oral mucosa, and that ex adiuvantibus therapy with probiotics can be employed to modify the natural course of the aphthous-like ulcers

    Bacteroides thetaiotaomicron Ameliorates Colon Inflammation in Preclinical Models of Crohn's Disease

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    SUPPLEMENTARY DATA: Supplementary data is available at Inflammatory Bowel Diseases onlinePeer reviewedPublisher PD
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