Defective Expression of Scavenger Receptors in Celiac Disease Mucosa

Celiac disease (CD) is a gluten sensitive enteropathy characterized by a marked infiltration of the mucosa with immune cells, over-production of inflammatory cytokines and epithelial cell damage. The factors/mechanisms that sustain and amplify the ongoing mucosal inflammation in CD are not however f...

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Main Authors: Cupi, Maria Laura, Sarra, Massimiliano, De Nitto, Daniela, Franzè, Eleonora, Marafini, Irene, Monteleone, Ivan, Del Vecchio Blanco, Giovanna, Paoluzi, Omero Alessandro, Di Fusco, Davide, Gentileschi, Paolo, Ortenzi, Angela, Colantoni, Alfredo, Pallone, Francesco, Monteleone, Giovanni
Format: Online
Language:English
Published: Public Library of Science 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074117/
id pubmed-4074117
recordtype oai_dc
spelling pubmed-40741172014-07-02 Defective Expression of Scavenger Receptors in Celiac Disease Mucosa Cupi, Maria Laura Sarra, Massimiliano De Nitto, Daniela Franzè, Eleonora Marafini, Irene Monteleone, Ivan Del Vecchio Blanco, Giovanna Paoluzi, Omero Alessandro Di Fusco, Davide Gentileschi, Paolo Ortenzi, Angela Colantoni, Alfredo Pallone, Francesco Monteleone, Giovanni Research Article Celiac disease (CD) is a gluten sensitive enteropathy characterized by a marked infiltration of the mucosa with immune cells, over-production of inflammatory cytokines and epithelial cell damage. The factors/mechanisms that sustain and amplify the ongoing mucosal inflammation in CD are not however fully understood. Here, we have examined whether in CD there is a defective clearance of apoptotic cells/bodies, a phenomenon that helps promote tolerogenic signals thus liming pathogenic responses. Accumulation of apoptotic cells and bodies was more pronounced in the epithelial and lamina propria compartments of active CD patients as compared to inactive CD patients and normal controls. Expression of scavenger receptors, which are involved in the clearance of apoptotic cells/bodies, namely thrombospondin (TSP)-1, CD36 and CD61, was significantly reduced in active CD as compared to inactive CD and normal mucosal samples. Consistently, lamina propria mononuclear cells (LPMC) of active CD patients had diminished ability to phagocyte apoptotic cells. Interleukin (IL)-15, IL-21 and interferon-γ, cytokines over-produced in active CD, inhibited the expression of TSP-1, CD36, and CD61 in normal intestinal LPMC. These results indicate that CD-related inflammation is marked by diminished clearance of apoptotic cells/bodies, thus suggesting a role for such a defect in the ongoing mucosal inflammation in this disorder. Public Library of Science 2014-06-27 /pmc/articles/PMC4074117/ /pubmed/24971453 http://dx.doi.org/10.1371/journal.pone.0100980 Text en © 2014 Cupi et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Cupi, Maria Laura
Sarra, Massimiliano
De Nitto, Daniela
Franzè, Eleonora
Marafini, Irene
Monteleone, Ivan
Del Vecchio Blanco, Giovanna
Paoluzi, Omero Alessandro
Di Fusco, Davide
Gentileschi, Paolo
Ortenzi, Angela
Colantoni, Alfredo
Pallone, Francesco
Monteleone, Giovanni
spellingShingle Cupi, Maria Laura
Sarra, Massimiliano
De Nitto, Daniela
Franzè, Eleonora
Marafini, Irene
Monteleone, Ivan
Del Vecchio Blanco, Giovanna
Paoluzi, Omero Alessandro
Di Fusco, Davide
Gentileschi, Paolo
Ortenzi, Angela
Colantoni, Alfredo
Pallone, Francesco
Monteleone, Giovanni
Defective Expression of Scavenger Receptors in Celiac Disease Mucosa
author_facet Cupi, Maria Laura
Sarra, Massimiliano
De Nitto, Daniela
Franzè, Eleonora
Marafini, Irene
Monteleone, Ivan
Del Vecchio Blanco, Giovanna
Paoluzi, Omero Alessandro
Di Fusco, Davide
Gentileschi, Paolo
Ortenzi, Angela
Colantoni, Alfredo
Pallone, Francesco
Monteleone, Giovanni
author_sort Cupi, Maria Laura
title Defective Expression of Scavenger Receptors in Celiac Disease Mucosa
title_short Defective Expression of Scavenger Receptors in Celiac Disease Mucosa
title_full Defective Expression of Scavenger Receptors in Celiac Disease Mucosa
title_fullStr Defective Expression of Scavenger Receptors in Celiac Disease Mucosa
title_full_unstemmed Defective Expression of Scavenger Receptors in Celiac Disease Mucosa
title_sort defective expression of scavenger receptors in celiac disease mucosa
description Celiac disease (CD) is a gluten sensitive enteropathy characterized by a marked infiltration of the mucosa with immune cells, over-production of inflammatory cytokines and epithelial cell damage. The factors/mechanisms that sustain and amplify the ongoing mucosal inflammation in CD are not however fully understood. Here, we have examined whether in CD there is a defective clearance of apoptotic cells/bodies, a phenomenon that helps promote tolerogenic signals thus liming pathogenic responses. Accumulation of apoptotic cells and bodies was more pronounced in the epithelial and lamina propria compartments of active CD patients as compared to inactive CD patients and normal controls. Expression of scavenger receptors, which are involved in the clearance of apoptotic cells/bodies, namely thrombospondin (TSP)-1, CD36 and CD61, was significantly reduced in active CD as compared to inactive CD and normal mucosal samples. Consistently, lamina propria mononuclear cells (LPMC) of active CD patients had diminished ability to phagocyte apoptotic cells. Interleukin (IL)-15, IL-21 and interferon-γ, cytokines over-produced in active CD, inhibited the expression of TSP-1, CD36, and CD61 in normal intestinal LPMC. These results indicate that CD-related inflammation is marked by diminished clearance of apoptotic cells/bodies, thus suggesting a role for such a defect in the ongoing mucosal inflammation in this disorder.
publisher Public Library of Science
publishDate 2014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074117/
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