Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease

Abstract Recently the role of Parkinson’s disease 7 (PARK7) was studied in gastrointestinal diseases, however, the complex role of PARK7 in the intestinal inflammation is still not completely clear. Expression and localization of PARK7 were determined in the colon biopsies of children with inflammat...

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Autores principales:	Rita Lippai, Apor Veres-Székely, Erna Sziksz, Yoichiro Iwakura, Domonkos Pap, Réka Rokonay, Beáta Szebeni, Gábor Lotz, Nóra J. Béres, Áron Cseh, Attila J. Szabó, Ádám Vannay
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8524719dc8ea4121b6f38ca873d01438
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spelling	oai:doaj.org-article:8524719dc8ea4121b6f38ca873d014382021-12-02T16:14:03ZImmunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease10.1038/s41598-021-93671-12045-2322https://doaj.org/article/8524719dc8ea4121b6f38ca873d014382021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-93671-1https://doaj.org/toc/2045-2322Abstract Recently the role of Parkinson’s disease 7 (PARK7) was studied in gastrointestinal diseases, however, the complex role of PARK7 in the intestinal inflammation is still not completely clear. Expression and localization of PARK7 were determined in the colon biopsies of children with inflammatory bowel disease (IBD), in the colon of dextran sodium sulphate (DSS) treated mice and in HT-29 colonic epithelial cells treated with interleukin (IL)-17, hydrogen peroxide (H2O2), tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β or lipopolysaccharide (LPS). Effect of PARK7 on the synthesis of IBD related cytokines was determined using PARK7 gene silenced HT-29 cells and 3,4,5-trimethoxy-N-(4-(8-methylimidazo(1,2-a)pyridine-2-yl)phenyl)benzamide (Comp23)—compound increasing PARK7 activity—treated mice with DSS-colitis. PARK7 expression was higher in the mucosa of children with Crohn’s disease compared to that of controls. While H2O2 and IL-17 treatment increased, LPS, TNF-α or TGF-β treatment decreased the PARK7 synthesis of HT-29 cells. PARK7 gene silencing influenced the synthesis of IL1B, IL6, TNFA and TGFB1 in vitro. Comp23 treatment attenuated the ex vivo permeability of colonic sacs, the clinical symptoms, and mucosal expression of Tgfb1, Il1b, Il6 and Il10 of DSS-treated mice. Our study revealed the role of PARK7 in the regulation of IBD-related inflammation in vitro and in vivo, suggesting its importance as a future therapeutic target.Rita LippaiApor Veres-SzékelyErna SzikszYoichiro IwakuraDomonkos PapRéka RokonayBeáta SzebeniGábor LotzNóra J. BéresÁron CsehAttila J. SzabóÁdám VannayNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Rita Lippai Apor Veres-Székely Erna Sziksz Yoichiro Iwakura Domonkos Pap Réka Rokonay Beáta Szebeni Gábor Lotz Nóra J. Béres Áron Cseh Attila J. Szabó Ádám Vannay Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease
description	Abstract Recently the role of Parkinson’s disease 7 (PARK7) was studied in gastrointestinal diseases, however, the complex role of PARK7 in the intestinal inflammation is still not completely clear. Expression and localization of PARK7 were determined in the colon biopsies of children with inflammatory bowel disease (IBD), in the colon of dextran sodium sulphate (DSS) treated mice and in HT-29 colonic epithelial cells treated with interleukin (IL)-17, hydrogen peroxide (H2O2), tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β or lipopolysaccharide (LPS). Effect of PARK7 on the synthesis of IBD related cytokines was determined using PARK7 gene silenced HT-29 cells and 3,4,5-trimethoxy-N-(4-(8-methylimidazo(1,2-a)pyridine-2-yl)phenyl)benzamide (Comp23)—compound increasing PARK7 activity—treated mice with DSS-colitis. PARK7 expression was higher in the mucosa of children with Crohn’s disease compared to that of controls. While H2O2 and IL-17 treatment increased, LPS, TNF-α or TGF-β treatment decreased the PARK7 synthesis of HT-29 cells. PARK7 gene silencing influenced the synthesis of IL1B, IL6, TNFA and TGFB1 in vitro. Comp23 treatment attenuated the ex vivo permeability of colonic sacs, the clinical symptoms, and mucosal expression of Tgfb1, Il1b, Il6 and Il10 of DSS-treated mice. Our study revealed the role of PARK7 in the regulation of IBD-related inflammation in vitro and in vivo, suggesting its importance as a future therapeutic target.
format	article
author	Rita Lippai Apor Veres-Székely Erna Sziksz Yoichiro Iwakura Domonkos Pap Réka Rokonay Beáta Szebeni Gábor Lotz Nóra J. Béres Áron Cseh Attila J. Szabó Ádám Vannay
author_facet	Rita Lippai Apor Veres-Székely Erna Sziksz Yoichiro Iwakura Domonkos Pap Réka Rokonay Beáta Szebeni Gábor Lotz Nóra J. Béres Áron Cseh Attila J. Szabó Ádám Vannay
author_sort	Rita Lippai
title	Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease
title_short	Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease
title_full	Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease
title_fullStr	Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease
title_full_unstemmed	Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease
title_sort	immunomodulatory role of parkinson’s disease 7 in inflammatory bowel disease
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/8524719dc8ea4121b6f38ca873d01438
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_version_	1718384359923253248

Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease

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