Inflammatory bowel disease: clinical aspects and treatments - PubMed (original) (raw)

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Inflammatory bowel disease: clinical aspects and treatments

Marc Fakhoury et al. J Inflamm Res. 2014.

Abstract

Inflammatory bowel disease (IBD) is defined as a chronic intestinal inflammation that results from host-microbial interactions in a genetically susceptible individual. IBDs are a group of autoimmune diseases that are characterized by inflammation of both the small and large intestine, in which elements of the digestive system are attacked by the body's own immune system. This inflammatory condition encompasses two major forms, known as Crohn's disease and ulcerative colitis. Patients affected by these diseases experience abdominal symptoms, including diarrhea, abdominal pain, bloody stools, and vomiting. Moreover, defects in intestinal epithelial barrier function have been observed in a number of patients affected by IBD. In this review, we first describe the types and symptoms of IBD and investigate the role that the epithelial barrier plays in the pathophysiology of IBD as well as the major cytokines involved. We then discuss steps used to diagnose this disease and the treatment options available, and finally provide an overview of the recent research that aims to develop new therapies for such chronic disorders.

Keywords: Crohn’s disease; cytokines; inflammatory bowel disease; ulcerative colitis.

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Figures

Figure 1

Figure 1

Triggering of immune response in Crohn’s disease. The main molecules involved are TGF-β, Tregs, TLR, DCs, Th cells, and TL1A. Note: Reprinted from Cobrin GM, Abreu MT. Defects in mucosal immunity leading to Crohn’s disease. Immunol Rev. 2005;206:277–295. Copyright © 2005, John Wiley and Sons. Abbreviations: DCs, dendritic cells; TGF-β, transforming growth factor beta; Tregs, regulatory T-cells; TLR, Toll-like receptors; Th, T-helper; TL1A, TNF-like ligand 1A; IL, interleukin; TNF-α, tumor necrosis factor alpha; IFN-γ, interferon gamma.

Figure 2

Figure 2

Factors determining T-lymphocyte differentiation in inflammatory bowel disease. Abbreviations: Th, T-helper; IL, interleukin; TNF-α, tumor necrosis factor alpha; IFN-γ, interferon gamma; NK, natural killer.

Figure 3

Figure 3

Granulomas in Crohn’s disease. Hematoxylin and eosin staining on the stomach shows gastric mucosal biopsy containing two characteristic granulomas (10×).

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References

    1. Ogura Y, Bonen DK, Inohara N, et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease. Nature. 2001;411:603–606. - PubMed
    1. Ponder A, Long DM. A clinical review of recent findings in the epidemiology of inflammatory bowel disease. Clin Epidemiol. 2013;5:237–247. - PMC - PubMed
    1. Weinstock JV, Summers R, Elliott DE. Helminths and harmony. Gut. 2004;53:7–9. - PMC - PubMed
    1. Shoda R, Matsueda K, Yamato S, Umeda N. Epidemiologic analysis of Crohn disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn disease in Japan. Am J Clin Nutr. 1996;64:741–745. - PubMed
    1. Hovde O, Moum B. Epidemiology and clinical course of Crohn’s disease: results from observational studies. World J Gastroenterol. 2012;18:1723–1731. - PMC - PubMed

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