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      Expression Pattern of Fatty Acid Binding Proteins in Celiac Disease Enteropathy

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          Abstract

          Celiac disease (CD) is an immune-mediated enteropathy that develops in genetically susceptible individuals following exposure to dietary gluten. Severe changes at the intestinal mucosa observed in untreated CD patients are linked to changes in the level and in the pattern of expression of different genes. Fully differentiated epithelial cells express two isoforms of fatty acid binding proteins (FABPs): intestinal and liver, IFABP and LFABP, respectively. These proteins bind and transport long chain fatty acids and also have other important biological roles in signaling pathways, particularly those related to PPAR γ and inflammatory processes. Herein, we analyze the serum levels of IFABP and characterize the expression of both FABPs at protein and mRNA level in small intestinal mucosa in severe enteropathy and normal tissue. As a result, we observed higher levels of circulating IFABP in untreated CD patients compared with controls and patients on gluten-free diet. In duodenal mucosa a differential FABPs expression pattern was observed with a reduction in mRNA levels compared to controls explained by the epithelium loss in severe enteropathy. In conclusion, we report changes in FABPs' expression pattern in severe enteropathy. Consequently, there might be alterations in lipid metabolism and the inflammatory process in the small intestinal mucosa.

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          Most cited references46

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          Cis elements of the villin gene control expression in restricted domains of the vertical (crypt) and horizontal (duodenum, cecum) axes of the intestine.

          Villin, an actin bundling protein found in the apical brush border of absorptive tissues, is one of the first structural genes to be transcriptionally activated in the embryonic intestinal endoderm. In the adult, villin is broadly expressed in every cell of the intestinal epithelium on both the vertical axis (crypt to villus tip) and the horizontal axis (duodenum through colon) of the intestine. Here, we document that a 12.4-kilobase region of the mouse villin gene drives high level expression of two different reporter genes (LacZ and Cre recombinase) within the entire intestinal epithelium of transgenic mice. Deletion of a portion of this transgene results in reduction of beta-galactosidase activity in restricted domains of the small intestine (duodenum) and large intestine (cecum). In addition, expression is reduced in the crypt compartment throughout the intestine. Thus, the global expression pattern of villin in the intestine is apparently the consequence of an amalgam of distinct and individual domain-specific control processes. That is, expression of villin in the duodenum and cecum requires different regulatory sequences than the rest of the intestine, and the expression of villin in crypts is regulated by different circuitry than expression of villin on villus tips.
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            American Gastroenterological Association (AGA) Institute technical review on the diagnosis and management of celiac disease.

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              Integration of genetic and immunological insights into a model of celiac disease pathogenesis.

              Celiac disease (CD) is a gluten-sensitive enteropathy that develops in genetically susceptible individuals by exposure to cereal gluten proteins. This review integrates insights from immunological studies with results of recent genetic genome-wide association studies into a disease model. Genetic data, among others, suggest that viral infections are implicated and that natural killer effector pathways are important in the pathogenesis of CD, but most prominently these data converge with existing immunological findings that CD is primarily a T cell-mediated immune disorder in which CD4(+) T cells that recognize gluten peptides in the context of major histocompatibility class II molecules play a central role. Comparison of genetic pathways as well as genetic susceptibility loci between CD and other autoimmune and inflammatory disorders reveals that CD bears stronger resemblance to T cell-mediated organ-specific autoimmune than to inflammatory diseases. Finally, we present evidence suggesting that the high prevalence of CD in modern societies may be the by-product of past selection for increased immune responses to combat infections in populations in which agriculture and cereals were introduced early on in the post-Neolithic period.
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                Author and article information

                Journal
                Mediators Inflamm
                Mediators Inflamm
                MI
                Mediators of Inflammation
                Hindawi Publishing Corporation
                0962-9351
                1466-1861
                2015
                5 August 2015
                : 2015
                : 738563
                Affiliations
                1Instituto de Investigaciones Bioquímicas de La Plata (INIBIOLP), CCT CONICET, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 1900 La Plata, Argentina
                2Departamento de Ciencias Biológicas, Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP), UNLP-CONICET, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, 1900 La Plata, Argentina
                3Laboratorio de Inmunología de Enfermedades Respiratorias, Instituto de Medicina Experimental (IMEX), CONICET, Academia Nacional de Medicina, C1425AUM Buenos Aires, Argentina
                4Servicio de Gastroenterología, Hospital de Niños “Sor María Ludovica”, 1900 La Plata, Argentina
                5Servicio de Gastroenterología, Hospital “San Martín”, 1900 La Plata, Argentina
                Author notes

                Academic Editor: Dezheng Zhao

                Article
                10.1155/2015/738563
                4540995
                26346822
                c7eef5d1-6ad1-4bdc-a204-edeebe7ceda2
                Copyright © 2015 Natalia M. Bottasso Arias et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 April 2015
                : 5 July 2015
                Categories
                Research Article

                Immunology
                Immunology

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