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Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease

Ulcerative colitis (UC) and Crohn’s Disease (CD) are chronic relapsing inflammatory diseases that are caused by genetic, environmental, and immune factors. Treatment strategies are currently based on symptomatic control by immunosuppression. The glucocorticoid-induced leucine zipper (GILZ), a mediat...

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Autores principales: Cari, Luigi, Rosati, Lucrezia, Leoncini, Giuseppe, Lusenti, Eleonora, Gentili, Marco, Nocentini, Giuseppe, Riccardi, Carlo, Migliorati, Graziella, Ronchetti, Simona
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9917296/
https://www.ncbi.nlm.nih.gov/pubmed/36768553
http://dx.doi.org/10.3390/ijms24032235
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author Cari, Luigi
Rosati, Lucrezia
Leoncini, Giuseppe
Lusenti, Eleonora
Gentili, Marco
Nocentini, Giuseppe
Riccardi, Carlo
Migliorati, Graziella
Ronchetti, Simona
author_facet Cari, Luigi
Rosati, Lucrezia
Leoncini, Giuseppe
Lusenti, Eleonora
Gentili, Marco
Nocentini, Giuseppe
Riccardi, Carlo
Migliorati, Graziella
Ronchetti, Simona
author_sort Cari, Luigi
collection PubMed
description Ulcerative colitis (UC) and Crohn’s Disease (CD) are chronic relapsing inflammatory diseases that are caused by genetic, environmental, and immune factors. Treatment strategies are currently based on symptomatic control by immunosuppression. The glucocorticoid-induced leucine zipper (GILZ), a mediator of several effects of glucocorticoids, was recently found to be secreted by goblet cells and play a role in inflammatory bowel disease (IBD). This study investigates which genes GILZ is associated with in its role in intestinal barrier functions. We examined datasets from the Gene Expression Omnibus (GEO) and ArrayExpress profiles of the gut of healthy subjects (HSs), as well as UC and CD patients. The human colonic epithelial HT29 cell line was used for in vitro validation experiments. GILZ was significantly correlated with MUC2, TLR2, and TLR4. In particular, an inverse correlation was found between the GILZ and MUC2 in HS and patients with IBD, mostly in those with an active disease. Further, direct pairwise correlations for GILZ/TLR2 and GILZ/TLR4 were found in HSs and UC patients, but not in CD patients. Overall, our results reveal the crosstalk at the transcription level between the GILZ, MUC2, and TLRs in the mucosal barrier through common pathways, and they open up new perspectives in terms of mucosal healing in IBD patients.
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spelling pubmed-99172962023-02-11 Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease Cari, Luigi Rosati, Lucrezia Leoncini, Giuseppe Lusenti, Eleonora Gentili, Marco Nocentini, Giuseppe Riccardi, Carlo Migliorati, Graziella Ronchetti, Simona Int J Mol Sci Article Ulcerative colitis (UC) and Crohn’s Disease (CD) are chronic relapsing inflammatory diseases that are caused by genetic, environmental, and immune factors. Treatment strategies are currently based on symptomatic control by immunosuppression. The glucocorticoid-induced leucine zipper (GILZ), a mediator of several effects of glucocorticoids, was recently found to be secreted by goblet cells and play a role in inflammatory bowel disease (IBD). This study investigates which genes GILZ is associated with in its role in intestinal barrier functions. We examined datasets from the Gene Expression Omnibus (GEO) and ArrayExpress profiles of the gut of healthy subjects (HSs), as well as UC and CD patients. The human colonic epithelial HT29 cell line was used for in vitro validation experiments. GILZ was significantly correlated with MUC2, TLR2, and TLR4. In particular, an inverse correlation was found between the GILZ and MUC2 in HS and patients with IBD, mostly in those with an active disease. Further, direct pairwise correlations for GILZ/TLR2 and GILZ/TLR4 were found in HSs and UC patients, but not in CD patients. Overall, our results reveal the crosstalk at the transcription level between the GILZ, MUC2, and TLRs in the mucosal barrier through common pathways, and they open up new perspectives in terms of mucosal healing in IBD patients. MDPI 2023-01-23 /pmc/articles/PMC9917296/ /pubmed/36768553 http://dx.doi.org/10.3390/ijms24032235 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Cari, Luigi
Rosati, Lucrezia
Leoncini, Giuseppe
Lusenti, Eleonora
Gentili, Marco
Nocentini, Giuseppe
Riccardi, Carlo
Migliorati, Graziella
Ronchetti, Simona
Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease
title Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease
title_full Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease
title_fullStr Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease
title_full_unstemmed Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease
title_short Association of GILZ with MUC2, TLR2, and TLR4 in Inflammatory Bowel Disease
title_sort association of gilz with muc2, tlr2, and tlr4 in inflammatory bowel disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9917296/
https://www.ncbi.nlm.nih.gov/pubmed/36768553
http://dx.doi.org/10.3390/ijms24032235
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